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LPS‐Induced Mitochondrial Damage via SLC41A1‐Mediated Magnesium Ion Efflux Leads to the Pyroptosis of Dental Stem Cells

Lipopolysaccharide induces upregulation of the magnesium (Mg2+) efflux transporter solute carrier family 41 member 1 in dental stem cells, leading to a decrease in intracellular Mg2+ concentration and promoting the binding of oligomycin sensitivity‐conferring protein and cyclophilinD. This enhances the sensitivity of mitochondrial permeability transition pore opening and triggers a cascade reaction that affects cell fate. Abstract Although regenerative endodontics demonstrate promise for dental pulp regeneration, chronic inflammation often hinders the success. This study aims to explore the mechanism whereby lipopolysaccharide (LPS) induces dental pulp regeneration failure. Transcriptomic profiling of LPS‐stimulated dental pulp stem cells (DPSCs) reveals dysregulated cation homeostasis and increased magnesium (Mg2⁺) transmembrane transport. Mechanistically, LPS is observed to activate the transcription factor signal transducer and activator of transcription 5A (STAT5A), which binds to the solute carrier family 41 member 1 (SLC41A1) promoter, thereby upregulating the Mg2⁺ efflux transporter and depleting intracellular Mg2⁺ levels. Mg2⁺ efflux destabilizes the mitochondrial permeability transition pore (mPTP), thus facilitating its opening via the interaction of oligomycin sensitivity‐conferring protein (OSCP) and cyclophilin D (CypD), which releases reactive oxygen species (ROS) and mitochondrial DNA (mtDNA) and exacerbates oxidative stress. The released mtDNA activates the absent in melanoma 2 (AIM2) inflammasome, thereby amplifying gasdermin D (GSDMD)‐mediated pyroptosis. Exogenous supplementation with Mg2⁺ restores intracellular Mg2⁺ homeostasis, suppresses mPTP opening, and reduces mtDNA and ROS leakage, thereby rescuing DPSCs viability and differentiation capacity. This study identifies SLC41A1‐mediated Mg2⁺ dysregulation as a pivotal driver of LPS‐induced mitochondrial damage and demonstrates that Mg2⁺ replenishment is a therapeutic strategy to counteract inflammation‐driven regenerative failure. Lipopolysaccharide induces upregulation of the magnesium (Mg 2+ ) efflux transporter solute carrier family 41 member 1 in dental stem cells, leading to a decrease in intracellular Mg 2+ concentration and promoting the binding of oligomycin sensitivity-conferring protein and cyclophilinD. This enhances the sensitivity of mitochondrial permeability transition pore opening and triggers a cascade reaction that affects cell fate. Abstract Although regenerative endodontics demonstrate promise for dental pulp regeneration, chronic inflammation often hinders the success. This study aims to explore the mechanism whereby lipopolysaccharide (LPS) induces dental pulp regeneration failure. Transcriptomic profiling of LPS-stimulated dental pulp stem cells (DPSCs) reveals dysregulated cation homeostasis and increased magnesium (Mg 2 ⁺) transmembrane transport. Mechanistically, LPS is observed to activate the transcription factor signal transducer and activator of transcription 5A (STAT5A), which binds to the solute carrier family 41 member 1 ( SLC41A1 ) promoter, thereby upregulating the Mg 2 ⁺ efflux transporter and depleting intracellular Mg 2 ⁺ levels. Mg 2 ⁺ efflux destabilizes the mitochondrial permeability transition pore (mPTP), thus facilitating its opening via the interaction of oligomycin sensitivity-conferring protein (OSCP) and cyclophilin D (CypD), which releases reactive oxygen species (ROS) and mitochondrial DNA (mtDNA) and exacerbates oxidative stress. The released mtDNA activates the absent in melanoma 2 (AIM2) inflammasome, thereby amplifying gasdermin D (GSDMD)-mediated pyroptosis. Exogenous supplementation with Mg 2 ⁺ restores intracellular Mg 2 ⁺ homeostasis, suppresses mPTP opening, and reduces mtDNA and ROS leakage, thereby rescuing DPSCs viability and differentiation capacity. This study identifies SLC41A1-mediated Mg 2 ⁺ dysregulation as a pivotal driver of LPS-induced mitochondrial damage and demonstrates that Mg 2 ⁺ replenishment is a therapeutic strategy to counteract inflammation-driven regenerative failure. Advanced Science, Volume 12, Issue 42, November 13, 2025.

Corticosterone Contributes to Context‐Triggered Retrieval of Morphine Withdrawal Memories by Acting on Basolateral Amygdala Neurons Projecting to Nucleus Accumbens Core

Context associated with morphine withdrawal elicits an increase in serum corticosterone levels. Corticosterone participates in CTR‐MWM by acting on MR, but not GR, in the BLA. MR in BLA→NAcC neurons mediates CTR‐MWM. MR increases presynaptic glutamate release and meanwhile participates in D1 receptor‐induced increases in presynaptic glutamate release and postsynaptic AMPA currents. MR increases the intrinsic excitability of BLA→NAcC neurons during CTR‐MWM. Abstract Context‐triggered retrieval of drug withdrawal memories (CTR‐DWM) is a major cause of drug relapse. Most studies of the context‐triggered retrieval of morphine withdrawal memories (CTR‐MWM) have mainly focused on the functional interactions within the central structures of the brain. It remains unknown how an increase in corticosterone, which is an important response under drug withdrawal state, participates in CTR‐MWM. The present results show that corticosterone contributes to CTR‐MWM; within the basolateral amygdala (BLA), it is the mineralocorticoid receptor (MR), rather than the glucocorticoid receptor (GR), activated by corticosterone that mediates CTR‐MWM; MR of BLA neurons projecting to the nucleus accumbens core (BLA→NAcC) mediates CTR‐MWM; MR increases presynaptic glutamate release and participates in dopamine D1 receptor ‐induced increase in presynaptic glutamate release and postsynaptic AMPA (α‐Amino‐3‐hydroxy‐5‐methyl‐4‐isoxazolepropionic Acid) currents; MR increases intrinsic excitability of BLA→NAcC neurons during CTR‐MWM. These results suggest that corticosterone contributes to CTR‐MWM by activating BLA→NAcC neurons through MR pathways, uncovering a link between a systemic hormonal response and a specific CTR‐MWM process. Context associated with morphine withdrawal elicits an increase in serum corticosterone levels. Corticosterone participates in CTR-MWM by acting on MR, but not GR, in the BLA. MR in BLA →NAcC neurons mediates CTR-MWM. MR increases presynaptic glutamate release and meanwhile participates in D1 receptor-induced increases in presynaptic glutamate release and postsynaptic AMPA currents. MR increases the intrinsic excitability of BLA →NAcC neurons during CTR-MWM. Abstract Context-triggered retrieval of drug withdrawal memories (CTR-DWM) is a major cause of drug relapse. Most studies of the context-triggered retrieval of morphine withdrawal memories (CTR-MWM) have mainly focused on the functional interactions within the central structures of the brain. It remains unknown how an increase in corticosterone, which is an important response under drug withdrawal state, participates in CTR-MWM. The present results show that corticosterone contributes to CTR-MWM; within the basolateral amygdala (BLA), it is the mineralocorticoid receptor (MR), rather than the glucocorticoid receptor (GR), activated by corticosterone that mediates CTR-MWM; MR of BLA neurons projecting to the nucleus accumbens core (BLA →NAcC ) mediates CTR-MWM; MR increases presynaptic glutamate release and participates in dopamine D1 receptor -induced increase in presynaptic glutamate release and postsynaptic AMPA (α-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic Acid) currents; MR increases intrinsic excitability of BLA →NAcC neurons during CTR-MWM. These results suggest that corticosterone contributes to CTR-MWM by activating BLA →NAcC neurons through MR pathways, uncovering a link between a systemic hormonal response and a specific CTR-MWM process. Advanced Science, Volume 12, Issue 42, November 13, 2025.

A Compartmentalized Joint‐on‐chip (JoC) Model to Unravel the Contribution of Cartilage and Synovium to Osteoarthritis Pathogenesis

A compartmentalized joint‐on‐chip (JoC) platform is here developed, modelling the interactions between cartilage and synovium in osteoarthritis (OA). Using independent culture and mechanical/biochemical stimulation, the JoC revealed how inflammation and mechanical damage drive mutual tissue changes. This tool offers new insights into OA onset and potential therapeutic targets by replicating complex joint dynamics in a controlled environment. Abstract Osteoarthritis (OA) is a joint disorder causing pain and disability, yet effective treatments are limited due to incomplete understanding of pathogenic mechanisms involving complex tissue interactions. Articular cartilage degradation is a hallmark, resulting from an imbalance in extracellular matrix turnover, influenced by mechanical and biochemical signals. The synovium also plays a central role in joint inflammation, with macrophages and fibroblasts releasing pro‐inflammatory cytokines and degradative enzymes. However, understanding cartilage‐synovium interactions in OA pathogenesis remains challenging. Here, a compartmentalized joint‐on‐chip (JoC) model that enables independent culture of 3D human cartilage and synovium constructs, allowing spatio‐temporal control over their communication, is presented. The JoC platform supports induction of OA characteristics in both tissues, by applying hyper‐physiological compression to cartilage constructs to mimic mechanical damage and by treating synovium constructs with TNFα and IFNγ to simulate inflammation. Moreover, the platform enables exploration of paracrine signaling between these tissues under pathophysiological conditions, showing that inflamed synovium constructs induce early cartilage degradation, while mechanically damaged cartilage promotes macrophage activation and inflammatory responses in the synovium. These findings support a bidirectional relationship in OA onset and underscore the JoC model as a tool for studying joint tissue interactions. A compartmentalized joint-on-chip (JoC) platform is here developed, modelling the interactions between cartilage and synovium in osteoarthritis (OA). Using independent culture and mechanical/biochemical stimulation, the JoC revealed how inflammation and mechanical damage drive mutual tissue changes. This tool offers new insights into OA onset and potential therapeutic targets by replicating complex joint dynamics in a controlled environment. Abstract Osteoarthritis (OA) is a joint disorder causing pain and disability, yet effective treatments are limited due to incomplete understanding of pathogenic mechanisms involving complex tissue interactions. Articular cartilage degradation is a hallmark, resulting from an imbalance in extracellular matrix turnover, influenced by mechanical and biochemical signals. The synovium also plays a central role in joint inflammation, with macrophages and fibroblasts releasing pro-inflammatory cytokines and degradative enzymes. However, understanding cartilage-synovium interactions in OA pathogenesis remains challenging. Here, a compartmentalized joint-on-chip (JoC) model that enables independent culture of 3D human cartilage and synovium constructs, allowing spatio-temporal control over their communication, is presented. The JoC platform supports induction of OA characteristics in both tissues, by applying hyper-physiological compression to cartilage constructs to mimic mechanical damage and by treating synovium constructs with TNFα and IFNγ to simulate inflammation. Moreover, the platform enables exploration of paracrine signaling between these tissues under pathophysiological conditions, showing that inflamed synovium constructs induce early cartilage degradation, while mechanically damaged cartilage promotes macrophage activation and inflammatory responses in the synovium. These findings support a bidirectional relationship in OA onset and underscore the JoC model as a tool for studying joint tissue interactions. Advanced Science, Volume 12, Issue 42, November 13, 2025.

Cracking the Valence Code: Patterned Facial Kinematics and Neural Signatures of Emotional Expressions in Mice

An AI‐powered system decodes emotional valence from mouse facial expressions, identifying ear dynamics as key indicators. By integrating facial kinematics with synchronized neural recordings, this approach establishes a direct link between behavior and brain activity, advancing automated emotion recognition in animal models. Abstract Despite advances in linking mouse facial expressions to emotional states, the specific facial features and neural signatures remain elusive. An artificial intelligence (AI)‐based framework that decodes mouse facial expressions is presented, revealing stable valence and arousal dimensions analogous to those described in human emotion models. Facial expressions emerge as robust indicators of positive and negative emotional responses, validated through pharmacological manipulations, while responses to hallucinogens highlight the potential of valence‐specific prototype modeling for interpreting previously uncharacterized emotional states. Using automated multikeypoint tracking, patterned facial kinematics that are consistent within the same emotional valence are identified. Ear dynamics, in particular, emerge as critical features, offering distinct and sensitive markers of subtle emotional distinctions. Neurocorrelational analyses and optogenetic inhibition targeting the ventral tegmental area further demonstrate the intricate link between facial expressions and valence‐specific neural activity in dopaminergic and GABAergic neurons. These findings establish a precise, high‐temporal‐resolution platform for objectively decoding murine emotional states, advancing the understanding of emotional processing mechanisms and informing the development of mood‐regulating therapies. An AI-powered system decodes emotional valence from mouse facial expressions, identifying ear dynamics as key indicators. By integrating facial kinematics with synchronized neural recordings, this approach establishes a direct link between behavior and brain activity, advancing automated emotion recognition in animal models. Abstract Despite advances in linking mouse facial expressions to emotional states, the specific facial features and neural signatures remain elusive. An artificial intelligence (AI)-based framework that decodes mouse facial expressions is presented, revealing stable valence and arousal dimensions analogous to those described in human emotion models. Facial expressions emerge as robust indicators of positive and negative emotional responses, validated through pharmacological manipulations, while responses to hallucinogens highlight the potential of valence-specific prototype modeling for interpreting previously uncharacterized emotional states. Using automated multikeypoint tracking, patterned facial kinematics that are consistent within the same emotional valence are identified. Ear dynamics, in particular, emerge as critical features, offering distinct and sensitive markers of subtle emotional distinctions. Neurocorrelational analyses and optogenetic inhibition targeting the ventral tegmental area further demonstrate the intricate link between facial expressions and valence-specific neural activity in dopaminergic and GABAergic neurons. These findings establish a precise, high-temporal-resolution platform for objectively decoding murine emotional states, advancing the understanding of emotional processing mechanisms and informing the development of mood-regulating therapies. Advanced Science, Volume 12, Issue 42, November 13, 2025.

Marker Metabolite‐Based Multi‐Omics Analysis Identifies New Loci Controlling Thousand Seed Weight in Brassica Napus

Marker metabolite‐based multi‐omics (genome, transcriptome, and metabolome) analysis is conducted firstly to unravel the genetic basis of thousand seed weight (TSW) in Brassica napus. The released metabolite‐QTL‐gene network represents a valuable genetic resource, and the newly validated BnaTGA6 is a promising target for the improvement of TSW in Brassica napus. Abstract The thousand seed weight (TSW) of Brassica napus (B. napus) is a crucial agronomic trait, and metabolites serve as a bridge between genotype and phenotype. Leveraging previously released metabolome data from a 388 B. napus population, 137 marker metabolites significantly correlated with TSW are identified, and 21 markers significantly correlate with both TSW and seed oil content. To delve deeper into the relationships between selected marker metabolites and phenotypes, a comprehensive multi‐omics analysis is conducted, which unveils 734 metabolite‐QTLs, 5,225 expression‐QTLs, and 9,077 transcriptome‐wide significantly associated genes. Employing weighted correlation network analysis, a triple‐link network is constructed involving 133 metabolites, 731 QTLs, and 3,321 genes. The multi‐omics analysis highlights the impact of the transcriptional factor TGACG motif‐binding factor 6 (BnaA03.TGA6) on TSW. Functional validation experiments with tga6 CRISPR/Cas9 mutants demonstrate larger seeds and altered associated metabolites levels compared to the wild type. RNA Sequencing, dual‐luciferase assay, Cleavage Under Targets and Tagmentation, and Electrophoretic Mobility Shift Assay results confirm that BnaA03.TGA6 activates the expression of E3 ubiquitin‐protein ligase DA2. In conclusion, this study is the first marker metabolite‐based multi‐omics analysis in unraveling the genetic basis of TSW in crop and identifying BnaA03.TGA6 as a novel gene negatively influencing TSW in B. napus. Marker metabolite-based multi-omics (genome, transcriptome, and metabolome) analysis is conducted firstly to unravel the genetic basis of thousand seed weight (TSW) in Brassica napus. The released metabolite-QTL-gene network represents a valuable genetic resource, and the newly validated BnaTGA6 is a promising target for the improvement of TSW in Brassica napus. Abstract The thousand seed weight (TSW) of Brassica napus ( B. napus ) is a crucial agronomic trait, and metabolites serve as a bridge between genotype and phenotype. Leveraging previously released metabolome data from a 388 B. napus population, 137 marker metabolites significantly correlated with TSW are identified, and 21 markers significantly correlate with both TSW and seed oil content. To delve deeper into the relationships between selected marker metabolites and phenotypes, a comprehensive multi-omics analysis is conducted, which unveils 734 metabolite-QTLs, 5,225 expression-QTLs, and 9,077 transcriptome-wide significantly associated genes. Employing weighted correlation network analysis, a triple-link network is constructed involving 133 metabolites, 731 QTLs, and 3,321 genes. The multi-omics analysis highlights the impact of the transcriptional factor TGACG motif-binding factor 6 (BnaA03.TGA6) on TSW. Functional validation experiments with tga6 CRISPR/Cas9 mutants demonstrate larger seeds and altered associated metabolites levels compared to the wild type. RNA Sequencing, dual-luciferase assay, Cleavage Under Targets and Tagmentation, and Electrophoretic Mobility Shift Assay results confirm that BnaA03.TGA6 activates the expression of E3 ubiquitin-protein ligase DA2. In conclusion, this study is the first marker metabolite-based multi-omics analysis in unraveling the genetic basis of TSW in crop and identifying BnaA03.TGA6 as a novel gene negatively influencing TSW in B. napus. Advanced Science, Volume 12, Issue 42, November 13, 2025.

Perpendicular Magnetic Anisotropy in FeRh Thin Films with Coexisting Magnetic Phases

This work reveals the evolution of perpendicular magnetic anisotropy in FeRh thin films during the antiferromagnetic‐ferromagnetic phase transition. Temperature‐dependent measurements and magnetic domain imaging demonstrate reorientation of magnetic moments from out‐of‐plane to in‐plane, driven by competition between magnetocrystalline anisotropy and shape anisotropy. These findings demonstrate the potential of FeRh in tunable spintronic applications. Abstract The advantages of high integration density, energy efficiency, and enhanced stability make the realization of perpendicular magnetic anisotropy (PMA) in single‐layer films a crucial step toward the development of advanced spintronic devices. A theoretical study predicted that the magnetic easy axis of FeRh film would reorient from out‐of‐plane (OP) to in‐plane (IP) directions during the antiferromagnetic‐ferromagnetic (AF‐FM) phase transition. However, few studies have observed an OP magnetic anisotropy in FeRh films. In this work, a continuous reorientation of the magnetic easy axis from OP to IP directions in FeRh film during its AF‐FM phase transition is demonstrated. Additionally, the anisotropy transition temperature increases with the film thickness. According to the magnetic domain imaging, the nucleation and initial growth of the FM domains at the AF state are dominated by magnetocrystalline anisotropy, leading to an OP easy axis in the FeRh thin film. With increasing temperature, shape anisotropy progressively dominates the magnetic properties of FeRh film, shifting the magnetic easy axis from OP to IP orientations. These findings not only demonstrate a novel anisotropy transition behavior in FeRh films, but also successfully induce PMA in such thick single‐layer films, providing critical experimental insights for the application of FeRh in spintronic devices. This work reveals the evolution of perpendicular magnetic anisotropy in FeRh thin films during the antiferromagnetic-ferromagnetic phase transition. Temperature-dependent measurements and magnetic domain imaging demonstrate reorientation of magnetic moments from out-of-plane to in-plane, driven by competition between magnetocrystalline anisotropy and shape anisotropy. These findings demonstrate the potential of FeRh in tunable spintronic applications. Abstract The advantages of high integration density, energy efficiency, and enhanced stability make the realization of perpendicular magnetic anisotropy (PMA) in single-layer films a crucial step toward the development of advanced spintronic devices. A theoretical study predicted that the magnetic easy axis of FeRh film would reorient from out-of-plane (OP) to in-plane (IP) directions during the antiferromagnetic-ferromagnetic (AF-FM) phase transition. However, few studies have observed an OP magnetic anisotropy in FeRh films. In this work, a continuous reorientation of the magnetic easy axis from OP to IP directions in FeRh film during its AF-FM phase transition is demonstrated. Additionally, the anisotropy transition temperature increases with the film thickness. According to the magnetic domain imaging, the nucleation and initial growth of the FM domains at the AF state are dominated by magnetocrystalline anisotropy, leading to an OP easy axis in the FeRh thin film. With increasing temperature, shape anisotropy progressively dominates the magnetic properties of FeRh film, shifting the magnetic easy axis from OP to IP orientations. These findings not only demonstrate a novel anisotropy transition behavior in FeRh films, but also successfully induce PMA in such thick single-layer films, providing critical experimental insights for the application of FeRh in spintronic devices. Advanced Science, Volume 12, Issue 42, November 13, 2025.

Inhibition of Hypersialylation in Human Intervertebral Disc Degeneration Modulates Inflammation and Metabolism

Glycosylation, specifically hypersialylation, is identified as a critical factor in human intervertebral disc (IVD) degeneration—a major cause of low back pain. This study demonstrates that inhibiting sialylation reduces inflammation and oxidative stress in IVD tissues, suggesting new therapeutic possibilities. These findings highlight glycan modifications as promising targets for improving outcomes in degenerative disc diseases. Abstract Intervertebral disc (IVD) degeneration is a major cause of low back pain (LBP), a significant global health burden. While glycosylation plays a key role in cellular signaling and inflammation, its role in IVD degeneration remains poorly understood. This study characterizes glycan alterations in human healthy and degenerated IVDs using glycomic (UPLC‐MS, MALDI‐IMS) and proteomic (LC‐MS) analyses, combined with functional studies. These results identify hypersialylation, especially α‐2,6‐linked sialic acid, as a prominent feature of degenerated IVDs. In vitro inhibition of sialylation (3Fax‐peracetyl Neu5Ac) in nucleus pulposus cells demonstrates reduced oxidative stress and inflammatory signaling, indicating a functional role for hypersialylation in IVD pathology. Targeting glycosylation pathways, notably sialylation, emerges as a promising therapeutic strategy for IVD degeneration. Glycosylation, specifically hypersialylation, is identified as a critical factor in human intervertebral disc (IVD) degeneration—a major cause of low back pain. This study demonstrates that inhibiting sialylation reduces inflammation and oxidative stress in IVD tissues, suggesting new therapeutic possibilities. These findings highlight glycan modifications as promising targets for improving outcomes in degenerative disc diseases. Abstract Intervertebral disc (IVD) degeneration is a major cause of low back pain (LBP), a significant global health burden. While glycosylation plays a key role in cellular signaling and inflammation, its role in IVD degeneration remains poorly understood. This study characterizes glycan alterations in human healthy and degenerated IVDs using glycomic (UPLC-MS, MALDI-IMS) and proteomic (LC-MS) analyses, combined with functional studies. These results identify hypersialylation, especially α-2,6-linked sialic acid, as a prominent feature of degenerated IVDs. In vitro inhibition of sialylation (3Fax-peracetyl Neu5Ac) in nucleus pulposus cells demonstrates reduced oxidative stress and inflammatory signaling, indicating a functional role for hypersialylation in IVD pathology. Targeting glycosylation pathways, notably sialylation, emerges as a promising therapeutic strategy for IVD degeneration. Advanced Science, EarlyView.

Tailoring Precursor‐Solvent Coordination Controls the Crystallization Kinetics and Nuclei Growth for Phase Homogenization in Wide‐Bandgap Perovskite Solar Cells

Volatile ammonium chloride (AC) regulates precursor‐solvent coordination and destabilizes hexagonal polytypes, promoting cubic‐phase formation and in situ defect self‐elimination in 1.73 eV wide‐bandgap perovskites. AC induces a de‐intercalated high‐valence iodoplumbate complex that suppresses the sol–gel state and balances nucleation, while Cl‐rich intermediates and NH4+−Cs+/FA+$N{H}_{4}^{+}-C{s}^{+}/F{A}^{+}$ cation exchange slow crystal growth, yielding devices with improved performance and excellent photostability. Abstract Wide‐bandgap (WBG) perovskites are promising top‐cell absorbers for tandem photovoltaics but suffer from unbalanced nucleation‐growth driven by strong coordination between polar aprotic solvents and perovskite precursors. This promotes the formation of hexagonal intermediate polytypes, stacking defects, halide‐cation migration, and phase segregation. Although long‐chain alkyl ammonium chlorides are used to control crystallization, the role of volatile ammonium chloride (AC) in altering the precursor chemistry and crystallization pathways in WBG perovskites remains unexplored. Present study, shows that AC weakens precursor‐solvent coordination and destabilizes undesired hexagonal polytypes. In situ characterizations indicate that AC induces high‐valence, de‐intercalated solvated iodoplumbate complexes that inhibit the sol–gel state and balance nucleation‐growth kinetics. Concurrently, Cl‐rich intermediates provide heterogeneous nucleation sites and, via cation exchange between NH4+ and Cs+/FA+ ions, retard uncontrolled crystal growth. The combined effect suppresses the formation of undesired phases, promotes transformation to the cubic perovskite phase, and enables defect self‐elimination during crystallization, yielding more homogeneous, higher‐quality films. As a result, AC‐treated perovskite films yield high‐quality 1.73 eV WBG perovskite solar cells with ≈18% PCE and a high Voc of 1.22 V, along with enhanced photostability. Volatile ammonium chloride (AC) regulates precursor-solvent coordination and destabilizes hexagonal polytypes, promoting cubic-phase formation and in situ defect self-elimination in 1.73 eV wide-bandgap perovskites. AC induces a de-intercalated high-valence iodoplumbate complex that suppresses the sol–gel state and balances nucleation, while Cl-rich intermediates and NH4+−Cs+/FA+$N{H}_{4}^{+}-C{s}^{+}/F{A}^{+}$ cation exchange slow crystal growth, yielding devices with improved performance and excellent photostability. Abstract Wide-bandgap (WBG) perovskites are promising top-cell absorbers for tandem photovoltaics but suffer from unbalanced nucleation-growth driven by strong coordination between polar aprotic solvents and perovskite precursors. This promotes the formation of hexagonal intermediate polytypes, stacking defects, halide-cation migration, and phase segregation. Although long-chain alkyl ammonium chlorides are used to control crystallization, the role of volatile ammonium chloride (AC) in altering the precursor chemistry and crystallization pathways in WBG perovskites remains unexplored. Present study, shows that AC weakens precursor-solvent coordination and destabilizes undesired hexagonal polytypes. In situ characterizations indicate that AC induces high-valence, de-intercalated solvated iodoplumbate complexes that inhibit the sol–gel state and balance nucleation-growth kinetics. Concurrently, Cl-rich intermediates provide heterogeneous nucleation sites and, via cation exchange between NH 4 + and Cs + /FA + ions, retard uncontrolled crystal growth. The combined effect suppresses the formation of undesired phases, promotes transformation to the cubic perovskite phase, and enables defect self-elimination during crystallization, yielding more homogeneous, higher-quality films. As a result, AC-treated perovskite films yield high-quality 1.73 eV WBG perovskite solar cells with ≈18% PCE and a high V oc of 1.22 V, along with enhanced photostability. Advanced Science, Volume 12, Issue 48, December 29, 2025.

Programmable Hydrogels: Frontiers in Dynamic Closed‐Loop Systems, Biomimetic Synergy, and Clinical Translation

This review summarizes the design principles and key features of programmable hydrogels that respond to multiple stimuli. It then delves into the cutting‐edge mechanisms of self‐executing systems, highlighting their role as the cornerstone of next‐generation programmable hydrogels (NGPHs). Finally, by addressing critical challenges in complexity and translation, the review looks to the future of NGPHs, emphasizing their evolution toward dynamic closed‐loop control, biomimetic intelligence, and successful clinical integration. Abstract Programmable hydrogels are an emerging class of intelligent materials engineered to respond precisely to specific stimuli, offering tailored functionalities with significant potential for biomedical applications, including drug delivery, tissue engineering, and wound healing. This review comprehensively explores various programmable hydrogels responsive to diverse triggers, including temperature, gene expression, color, shape, and mechanical force. The design and fabrication methods underlying these systems are detailed, highlighting the roles of crosslinkers, adhesion groups, and photosensitive functional groups. Furthermore, the key physical, chemical, and biological properties that govern the performance and functionality of hydrogels are analyzed. The review further examines the mechanisms and recent advancements in self‐executing hydrogels, such as self‐activated, self‐oxygenated, self‐expandable, and self‐powered systems, demonstrating how these innovative designs drive the development of next‐generation programmable hydrogels. The main challenges in hydrogel design, including complexity, reproducibility, and clinical translation, are also addressed. Finally, a perspective on future research directions, highlighting the integration of the latest technologies to realize programmable hydrogels with dynamic closed‐loop responsiveness, bionic synergy, and robust clinical applicability, is offered. This review summarizes the design principles and key features of programmable hydrogels that respond to multiple stimuli. It then delves into the cutting-edge mechanisms of self-executing systems, highlighting their role as the cornerstone of next-generation programmable hydrogels (NGPHs). Finally, by addressing critical challenges in complexity and translation, the review looks to the future of NGPHs, emphasizing their evolution toward dynamic closed-loop control, biomimetic intelligence, and successful clinical integration. Abstract Programmable hydrogels are an emerging class of intelligent materials engineered to respond precisely to specific stimuli, offering tailored functionalities with significant potential for biomedical applications, including drug delivery, tissue engineering, and wound healing. This review comprehensively explores various programmable hydrogels responsive to diverse triggers, including temperature, gene expression, color, shape, and mechanical force. The design and fabrication methods underlying these systems are detailed, highlighting the roles of crosslinkers, adhesion groups, and photosensitive functional groups. Furthermore, the key physical, chemical, and biological properties that govern the performance and functionality of hydrogels are analyzed. The review further examines the mechanisms and recent advancements in self-executing hydrogels, such as self-activated, self-oxygenated, self-expandable, and self-powered systems, demonstrating how these innovative designs drive the development of next-generation programmable hydrogels. The main challenges in hydrogel design, including complexity, reproducibility, and clinical translation, are also addressed. Finally, a perspective on future research directions, highlighting the integration of the latest technologies to realize programmable hydrogels with dynamic closed-loop responsiveness, bionic synergy, and robust clinical applicability, is offered. Advanced Science, EarlyView.

Nitrogen‐Boosted H2O2 Production of Arginine‐Polyphenol Nanozyme Drives Oxidative Eustress for Hair Regeneration

PEA nanoenzymes are assembled from L‐arginine and EGCG. The nitrogen element in arginine enhances the thermodynamic feasibility of H2O2 production through PEA's oxygen reduction catalysis, enabling nitrogen‐dependent H2O2 release. Intradermal delivery of PEA via microneedles promotes efficient H2O2 synthesis, thereby stimulating regrowth in telogen effluvium model. Abstract Reactive oxygen species (ROS)‐triggered oxidative eustress can stimulate regenerative signaling, yet its therapeutic window remains narrow. Mitochondrial respiratory complexes and superoxide dismutase (SOD) are canonical enzymatic sources of intracellular H2O2. Here we report a biomimetic polyphenol–amino acid nanozyme (PEAs) that couples the semiquinone radical of coenzyme Q (ubiquinone) with the Arg143 residue of Zn/Cu‐SOD1. Through self‐assembling epigallocatechin gallate (EGCG) and L‐arginine (L‐Arg), PEAs enable O2 adsorption and activation with controlled H2O2 generation. The H2O2 output is finely tuned by modulating the nitrogen (N) content from L‐Arg. Integrated experimental and computational analyses reveal that the N‐sites introduced by L‐Arg promote semiquinone electron delocalization, increase semiquinone abundance, thereby strengthening O2 adsorption, facilitating electron/proton transfer, and lowering the reaction barrier for H2O2 synthesis. Using the genetically encoded H2O2 sensor HyPerion, this work validates the sustained intracellular modulation of H2O2 by PEAs. In a mouse model of telogen effluvium, controlled H2O2 delivery activates the follicular niche via Wnt/β‐catenin upregulation and Ca2+/calcineurin/NFAT downregulation, resulting in robust follicle activation and a non‐pharmacological approach to alopecia therapy. This polyphenol–amino acid nanozyme therefore provides a safe and effective strategy for in vivo pro‐oxidative modulation, offering a tunable H2O2‐based platform to harness beneficial oxidative stress for tissue renewal. PEA nanoenzymes are assembled from L-arginine and EGCG. The nitrogen element in arginine enhances the thermodynamic feasibility of H 2 O 2 production through PEA's oxygen reduction catalysis, enabling nitrogen-dependent H 2 O 2 release. Intradermal delivery of PEA via microneedles promotes efficient H 2 O 2 synthesis, thereby stimulating regrowth in telogen effluvium model. Abstract Reactive oxygen species (ROS)-triggered oxidative eustress can stimulate regenerative signaling, yet its therapeutic window remains narrow. Mitochondrial respiratory complexes and superoxide dismutase (SOD) are canonical enzymatic sources of intracellular H 2 O 2. Here we report a biomimetic polyphenol–amino acid nanozyme (PEAs) that couples the semiquinone radical of coenzyme Q (ubiquinone) with the Arg143 residue of Zn/Cu-SOD1. Through self-assembling epigallocatechin gallate (EGCG) and L-arginine (L-Arg), PEAs enable O 2 adsorption and activation with controlled H 2 O 2 generation. The H 2 O 2 output is finely tuned by modulating the nitrogen (N) content from L-Arg. Integrated experimental and computational analyses reveal that the N-sites introduced by L-Arg promote semiquinone electron delocalization, increase semiquinone abundance, thereby strengthening O 2 adsorption, facilitating electron/proton transfer, and lowering the reaction barrier for H 2 O 2 synthesis. Using the genetically encoded H 2 O 2 sensor HyPerion, this work validates the sustained intracellular modulation of H 2 O 2 by PEAs. In a mouse model of telogen effluvium, controlled H 2 O 2 delivery activates the follicular niche via Wnt/β-catenin upregulation and Ca 2+ /calcineurin/NFAT downregulation, resulting in robust follicle activation and a non-pharmacological approach to alopecia therapy. This polyphenol–amino acid nanozyme therefore provides a safe and effective strategy for in vivo pro-oxidative modulation, offering a tunable H 2 O 2 -based platform to harness beneficial oxidative stress for tissue renewal. Advanced Science, EarlyView.

Carbene–Metal–Amide Materials Design: Tailoring π‐Extended Amides for High‐Performance Organic Light‐Emitting Diodes

Sky‐blue and green thermally activated delayed fluorescent emitters, carbene–gold–amides (CMA), possess near unity photoluminescent quantum yields and high radiative rates up to 2.1 × 106 s−1. Organic light‐emitting diodes (OLED) emit sky‐blue electroluminescence with efficiency over 20%, including host‐free OLED architecture, with operating stability LT90 of 4.3 h at practical brightness 100 cd m−2. Abstract A series of gold‐centred carbene‐metal‐amide (CMA) complexes are prepared with a rigid benzofuroindole (BFI) and benzothioindole (BTI) amide donor ligands coordinated with bicyclic(alkyl)amino carbene (BiC)Au(I)‐moiety in high yields. CMA complexes emit in the sky‐blue range at 501 and 511 nm with unity quantum yields in amorphous solid state media. Both CMA complexes emit thermally activated delayed fluorescence (TADF) originating from a charge transfer (CT) state with an excited state lifetime as short as 473 ns, resulting in fast radiative rates of 2 × 106 s−1. The impact on the photoluminescence properties of the electron‐donating oxygen and sulfur atoms in amide‐donor ligand has been interpreted with the help of steady‐state and transient photo and electroluminescence experiments. Theoretical investigations revealed two charge‐transfer (T1 and T2) states followed by a locally excited T3 triplet state, and their spin–orbit coupling analysis. Sky‐blue host‐guest and host‐free organic light‐emitting diode (OLED) devices are fabricated with electroluminescence at ≈490 nm and practical external quantum efficiencies up to 23% with colour coordinates CIE (x; y) = 0.19; 0.32. The superior performance and operating stability of the neat OLEDs are correlated with the presence of the heavier sulfur atom, suggesting further molecular design modifications toward stable CMA OLED devices with a simplified architecture of the emitting layer (host‐free OLED). Sky-blue and green thermally activated delayed fluorescent emitters, carbene–gold–amides (CMA), possess near unity photoluminescent quantum yields and high radiative rates up to 2.1 × 10 6 s −1. Organic light-emitting diodes (OLED) emit sky-blue electroluminescence with efficiency over 20%, including host-free OLED architecture, with operating stability LT 90 of 4.3 h at practical brightness 100 cd m −2. Abstract A series of gold-centred carbene-metal-amide (CMA) complexes are prepared with a rigid benzofuroindole (BFI) and benzothioindole (BTI) amide donor ligands coordinated with bicyclic(alkyl)amino carbene (BiC)Au(I)-moiety in high yields. CMA complexes emit in the sky-blue range at 501 and 511 nm with unity quantum yields in amorphous solid state media. Both CMA complexes emit thermally activated delayed fluorescence (TADF) originating from a charge transfer (CT) state with an excited state lifetime as short as 473 ns, resulting in fast radiative rates of 2 × 10 6 s −1. The impact on the photoluminescence properties of the electron-donating oxygen and sulfur atoms in amide-donor ligand has been interpreted with the help of steady-state and transient photo and electroluminescence experiments. Theoretical investigations revealed two charge-transfer (T 1 and T 2 ) states followed by a locally excited T 3 triplet state, and their spin–orbit coupling analysis. Sky-blue host-guest and host-free organic light-emitting diode (OLED) devices are fabricated with electroluminescence at ≈490 nm and practical external quantum efficiencies up to 23% with colour coordinates CIE (x; y) = 0.19; 0.32. The superior performance and operating stability of the neat OLEDs are correlated with the presence of the heavier sulfur atom, suggesting further molecular design modifications toward stable CMA OLED devices with a simplified architecture of the emitting layer (host-free OLED). Advanced Science, EarlyView.

Plant Robotics for Sustainable and Environmentally Friendly Robots: Insights from Actuation Characteristics

Plants are promising materials for building sustainable and eco‐friendly robots due to their inherent multifunctionality, with actuation playing a crucial role. This article focuses on the physical movements of plants and, from the perspective of actuation characteristics, explores representative plant species and their behaviors, the current state of plant robots, and future prospects for this emerging field. Abstract Robots play an ever‐expanding role in society by performing a broad range of tasks. However, there are growing concerns about their environmental sustainability, as many conventional robotic systems rely on materials that are neither renewable nor degradable. Consequently, significant efforts are being made to develop eco‐friendly robots built from sustainable and biodegradable materials. In this context, plants represent a promising direction, as the biomaterials composing plants are biodegradable, and their inherent multifunctionality as living organisms, including sensing, actuation, energy harvesting, and self‐healing, makes them strong candidates for realizing biodegradable robotic systems. Moreover, they are abundant and renewable resources. Recent studies have demonstrated plant‐based robotic systems that harness some of these features, helping to establish plant robotics as an emerging research field. Among the many functions plants offer, actuation is pivotal, as it enables physical robotic motion, such as locomotion and grasping, which substantially broadens the potential applications of plant robots. Focusing on plant movement, this article reviews key plant species and their behaviors through the perspective of actuation characteristics. It also examines the current landscape of plant‐based robotic systems and outlines future research directions in this rapidly growing field. Plants are promising materials for building sustainable and eco-friendly robots due to their inherent multifunctionality, with actuation playing a crucial role. This article focuses on the physical movements of plants and, from the perspective of actuation characteristics, explores representative plant species and their behaviors, the current state of plant robots, and future prospects for this emerging field. Abstract Robots play an ever-expanding role in society by performing a broad range of tasks. However, there are growing concerns about their environmental sustainability, as many conventional robotic systems rely on materials that are neither renewable nor degradable. Consequently, significant efforts are being made to develop eco-friendly robots built from sustainable and biodegradable materials. In this context, plants represent a promising direction, as the biomaterials composing plants are biodegradable, and their inherent multifunctionality as living organisms, including sensing, actuation, energy harvesting, and self-healing, makes them strong candidates for realizing biodegradable robotic systems. Moreover, they are abundant and renewable resources. Recent studies have demonstrated plant-based robotic systems that harness some of these features, helping to establish plant robotics as an emerging research field. Among the many functions plants offer, actuation is pivotal, as it enables physical robotic motion, such as locomotion and grasping, which substantially broadens the potential applications of plant robots. Focusing on plant movement, this article reviews key plant species and their behaviors through the perspective of actuation characteristics. It also examines the current landscape of plant-based robotic systems and outlines future research directions in this rapidly growing field. Advanced Science, EarlyView.

Targeting Endothelial KDM5A to Attenuate Aging and Ameliorate Age‐Associated Metabolic Abnormalities

This study identifies endothelial KDM5A as a key regulator of aging. KDM5A deficiency accelerates aging by enhancing H3K4me3‐mediated FABP4 expression, disrupting fatty acid metabolism, and promoting multi‐organ senescence. KDM5A restoration or FABP4 inhibition reverses these adverse effects and extends lifespan, positioning the KDM5A/FABP4 axis as a potential therapeutic target for vascular aging and metabolic disorders. Abstract Vascular aging accelerates the gradual deterioration of systemic organ function, yet its key driving factors are still largely unexplored. Here, it is demonstrated that lysine‐specific demethylase 5A (KDM5A) decreases and histone H3 lysine 4 (H3K4me3) increases in vascular endothelial cells (VECs) isolated from ageing mice and VEC senescence models. KDM5A deficiency exacerbated endothelial cell aging in vitro. Endothelial‐specific KDM5A‐deficient mice exhibit shortened lifespan and multiple senescent phenotypes, including fat accumulation, reduced thermogenic capacity, skeletal kyphosis, and age‐related liver lesions, while maintaining VECs‐specific KDM5A levels attenuates these adverse metabolic abnormalities and prolongs lifespan. Mechanistically, endothelial KDM5A deficiency aggravates aging‐associated fatty acid (FA) metabolism disorders by enhancing H3K4me3 enrichment at the promoter region of FA‐binding protein 4 (FABP4), which leads to active FABP4 transcription. Together, the study reveals the regulatory mechanisms of KDM5A in age‐dependent metabolic disorders and identifies KDM5A/FABP4 axis as a potential therapeutic target for vascular aging and related organ dysfunction. This study identifies endothelial KDM5A as a key regulator of aging. KDM5A deficiency accelerates aging by enhancing H3K4me3-mediated FABP4 expression, disrupting fatty acid metabolism, and promoting multi-organ senescence. KDM5A restoration or FABP4 inhibition reverses these adverse effects and extends lifespan, positioning the KDM5A/FABP4 axis as a potential therapeutic target for vascular aging and metabolic disorders. Abstract Vascular aging accelerates the gradual deterioration of systemic organ function, yet its key driving factors are still largely unexplored. Here, it is demonstrated that lysine-specific demethylase 5A (KDM5A) decreases and histone H3 lysine 4 (H3K4me3) increases in vascular endothelial cells (VECs) isolated from ageing mice and VEC senescence models. KDM5A deficiency exacerbated endothelial cell aging in vitro. Endothelial-specific KDM5A-deficient mice exhibit shortened lifespan and multiple senescent phenotypes, including fat accumulation, reduced thermogenic capacity, skeletal kyphosis, and age-related liver lesions, while maintaining VECs-specific KDM5A levels attenuates these adverse metabolic abnormalities and prolongs lifespan. Mechanistically, endothelial KDM5A deficiency aggravates aging-associated fatty acid (FA) metabolism disorders by enhancing H3K4me3 enrichment at the promoter region of FA-binding protein 4 ( FABP4 ), which leads to active FABP4 transcription. Together, the study reveals the regulatory mechanisms of KDM5A in age-dependent metabolic disorders and identifies KDM5A/FABP4 axis as a potential therapeutic target for vascular aging and related organ dysfunction. Advanced Science, EarlyView.

A 3D Porous MXene/PNIPAAm Hydrogel Composite with Advanced Degradation Stability and Control of Electronic Properties in Air

This paper reports a fundamental study of the mutual benefits of the components in an MXene/PNIPAAm hydrogel composite with regard to enhanced degradation stability and tailorable electronic properties. The presented work focuses on the investigation of the fundamental material properties and ways for their modification. Furthermore, a chemiresistive sensing mechanism is explored for a future application of volatile organic compound detection. Abstract This study reports the fundamental investigation of a composite material consisting of MXene (Ti3C2Tx) and a stimulus‐responsive hydrogel (Poly(N‐isopropylacrylamide)–PNIPAAm). Thereby, the fabrication and comparison of pure MXene and composite samples featuring either a compact or a highly porous 3D microstructure, reveal unique properties with respect to: i) controllable 3D spatial arrangement of MXene instead of the prevalent stacked‐sheet structure, ii) reduction of oxidation‐induced degradation of MXene and substantially enhanced stability over the course of three months for the composite, and iii) tunable electronic states in response to gas interactions. Material characterization is conducted by scanning electron microscopy and rheology to assess the microstructural and mechanical properties, and in a chemiresistive measurement setup for the determination of electrical properties and the evaluation of the composite's potential for VOC sensing in a gaseous environment with the test analyte acetone. These investigations reveal material effects and properties that address some of the key MXene‐related challenges. Additionally, the interplay between the MXene and the hydrogel enables unprecedented opportunities for enhancing the sensing potential of stimulus‐responsive hydrogels, specifically in gaseous environments. This paper reports a fundamental study of the mutual benefits of the components in an MXene/PNIPAAm hydrogel composite with regard to enhanced degradation stability and tailorable electronic properties. The presented work focuses on the investigation of the fundamental material properties and ways for their modification. Furthermore, a chemiresistive sensing mechanism is explored for a future application of volatile organic compound detection. Abstract This study reports the fundamental investigation of a composite material consisting of MXene (Ti 3 C 2 T x ) and a stimulus-responsive hydrogel (Poly(N-isopropylacrylamide)–PNIPAAm). Thereby, the fabrication and comparison of pure MXene and composite samples featuring either a compact or a highly porous 3D microstructure, reveal unique properties with respect to: i) controllable 3D spatial arrangement of MXene instead of the prevalent stacked-sheet structure, ii) reduction of oxidation-induced degradation of MXene and substantially enhanced stability over the course of three months for the composite, and iii) tunable electronic states in response to gas interactions. Material characterization is conducted by scanning electron microscopy and rheology to assess the microstructural and mechanical properties, and in a chemiresistive measurement setup for the determination of electrical properties and the evaluation of the composite's potential for VOC sensing in a gaseous environment with the test analyte acetone. These investigations reveal material effects and properties that address some of the key MXene-related challenges. Additionally, the interplay between the MXene and the hydrogel enables unprecedented opportunities for enhancing the sensing potential of stimulus-responsive hydrogels, specifically in gaseous environments. Advanced Science, EarlyView.

Improving Interlayer Interactions in Proton Exchange Membrane Fuel Cell through Carbon Nanotube‐Based Catalyst Design

This review highlights how carbon nanotube (CNT)–based catalyst designs enhance proton exchange membrane fuel cell (PEMFC) performance by improving interlayer interactions. Vertically aligned CNTs facilitate water management, mass transfer, and electron conduction while promoting effective active sites and reducing interfacial resistance. The integrative framework presented provides design principles for durable and efficient next‐generation PEMFC architecture. Abstract Proton exchange membrane fuel cells (PEMFCs) have gained significant attention due to their efficient use of hydrogen energy, high energy density, and zero emissions, making them ideal for future transportation and portable energy frameworks. Despite these advantages, challenges related to catalyst layer design, material durability, and cost‐effectiveness persist. This paper reviews recent advancements in the application of carbon nanotubes (CNTs) in PEMFCs. The study highlights the integration of CNTs at various levels of the membrane electrode assembly (MEA), focusing on both covalent and non‐covalent modification schemes. A particular emphasis is placed on vertically aligned carbon nanotube (VACNT) structures due to their potential to improve electron and mass transport pathways, leading to enhanced fuel cell performance and durability. Additionally, the synergistic effects of blending CNTs with carbon black (CB) are explored to address issues related to interlayer interactions and material conductivity. The review identifies gaps in current research, particularly in understanding the comprehensive impact of CNT modifications on the operational state of the MEA, and proposes new insights and strategies for material design aimed at facilitating the commercialization of PEMFC technology. This review highlights how carbon nanotube (CNT)–based catalyst designs enhance proton exchange membrane fuel cell (PEMFC) performance by improving interlayer interactions. Vertically aligned CNTs facilitate water management, mass transfer, and electron conduction while promoting effective active sites and reducing interfacial resistance. The integrative framework presented provides design principles for durable and efficient next-generation PEMFC architecture. Abstract Proton exchange membrane fuel cells (PEMFCs) have gained significant attention due to their efficient use of hydrogen energy, high energy density, and zero emissions, making them ideal for future transportation and portable energy frameworks. Despite these advantages, challenges related to catalyst layer design, material durability, and cost-effectiveness persist. This paper reviews recent advancements in the application of carbon nanotubes (CNTs) in PEMFCs. The study highlights the integration of CNTs at various levels of the membrane electrode assembly (MEA), focusing on both covalent and non-covalent modification schemes. A particular emphasis is placed on vertically aligned carbon nanotube (VACNT) structures due to their potential to improve electron and mass transport pathways, leading to enhanced fuel cell performance and durability. Additionally, the synergistic effects of blending CNTs with carbon black (CB) are explored to address issues related to interlayer interactions and material conductivity. The review identifies gaps in current research, particularly in understanding the comprehensive impact of CNT modifications on the operational state of the MEA, and proposes new insights and strategies for material design aimed at facilitating the commercialization of PEMFC technology. Advanced Science, EarlyView.