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GbWAKL20 Phosphorylates GbNFYB8 to Modulate Verticillium Wilt Resistance in Cotton

Wall‐associated receptor‐like kinases (WAKLs) play pivotal roles in extracellular–intracellular signal transduction. Upon sensing Verticillium dahliae infestation at the plasma membrane, GbWAKL20 accumulates and transmits signals to the nucleus via endoplasmic reticulum‐mediated Golgi vesicle transport. GbWAKL20 phosphorylates the transcription factor GbNFYB8 and promotes its nuclear translocation, greatly activating downstream defense responses and enhancing cotton resistance to V. dahliae. ABSTRACT Verticillium wilt (VW), caused by Verticillium dahliae (Vd), is a major threat to cotton production worldwide. Wall‐associated receptor‐like kinases (WAKLs) are critical for plant‐environment communication and fungal pathogen resistance, yet their regulatory mechanisms in cotton remain unclear. Through genomic and transcriptomic analysis, coupled with disease resistance assays, we identified a WAKL gene from Gossypium barbadense acc. Hai7124, named GbWAKL20, was involved in VW resistance. GbWAKL20 was significantly induced upon Vd infection. Silencing GbWAKL20 in Hai7124 compromised VW resistance, suppressed the mitogen‐activated protein kinase (MAPK) cascade and salicylic acid (SA) signaling pathway, whereas its ectopic overexpression in Arabidopsis enhanced immune responses. Upon sensing extracellular stress signals at the plasma membrane, GbWAKL20 accumulates and transmits these signals to the nucleus via endoplasmic reticulum‐mediated Golgi vesicle transport. GbWAKL20 interacts with the transcription factor GbNFYB8 and promotes its nuclear translocation through phosphorylation. GbNFYB8 binds to CCAAT elements in promoters of immunity‐related genes and activates their expression. Silencing GbNFYB8 reduces VW resistance in cotton. GbWAKL20‐mediated phosphorylation enhances transcriptional activation activity of GbNFYB8, further amplifying disease resistance responses and improving plant resistance. Our results highlight the significance of the GbWAKL20‐GbNFYB8 module in defending against VW and provide novel insights into plant immune signaling pathways. Wall-associated receptor-like kinases (WAKLs) play pivotal roles in extracellular–intracellular signal transduction. Upon sensing Verticillium dahliae infestation at the plasma membrane, GbWAKL20 accumulates and transmits signals to the nucleus via endoplasmic reticulum-mediated Golgi vesicle transport. GbWAKL20 phosphorylates the transcription factor GbNFYB8 and promotes its nuclear translocation, greatly activating downstream defense responses and enhancing cotton resistance to V. dahliae. ABSTRACT Verticillium wilt (VW), caused by Verticillium dahliae ( Vd ), is a major threat to cotton production worldwide. Wall-associated receptor-like kinases (WAKLs) are critical for plant-environment communication and fungal pathogen resistance, yet their regulatory mechanisms in cotton remain unclear. Through genomic and transcriptomic analysis, coupled with disease resistance assays, we identified a WAKL gene from Gossypium barbadense acc. Hai7124, named GbWAKL20, was involved in VW resistance. GbWAKL20 was significantly induced upon Vd infection. Silencing GbWAKL20 in Hai7124 compromised VW resistance, suppressed the mitogen-activated protein kinase (MAPK) cascade and salicylic acid (SA) signaling pathway, whereas its ectopic overexpression in Arabidopsis enhanced immune responses. Upon sensing extracellular stress signals at the plasma membrane, GbWAKL20 accumulates and transmits these signals to the nucleus via endoplasmic reticulum-mediated Golgi vesicle transport. GbWAKL20 interacts with the transcription factor GbNFYB8 and promotes its nuclear translocation through phosphorylation. GbNFYB8 binds to CCAAT elements in promoters of immunity-related genes and activates their expression. Silencing GbNFYB8 reduces VW resistance in cotton. GbWAKL20-mediated phosphorylation enhances transcriptional activation activity of GbNFYB8, further amplifying disease resistance responses and improving plant resistance. Our results highlight the significance of the GbWAKL20-GbNFYB8 module in defending against VW and provide novel insights into plant immune signaling pathways. Advanced Science, EarlyView.

Reconstructing Coherent Functional Landscape From Multi‐Modal Multi‐Slice Spatial Transcriptomics by a Variational Spatial Gaussian Process

This study introduces stVGP, a variational spatial Gaussian process framework for multi‐modal, multi‐slice spatial transcriptomics. By integrating histological and genomic data through hybrid alignment and attention‐based fusion, stVGP reconstructs coherent 3D functional landscapes. It enables virtual slice generation, cross‐modal gene prediction, and niche deciphering, providing a robust computational tool for mapping complex biological architectures. ABSTRACT Spatial transcriptomics (ST) technologies are revolutionizing our ability to investigate the spatial organization of complex tissues. While ST has significantly advanced our understanding of tissue architecture, most analytical approaches remain restricted to 2D sections, limiting insights into the full 3D spatial context. Here, we introduce stVGP, a variational spatial Gaussian process framework designed to align, integrate, and reconstruct spatial coherent domains from multi‐modal, multi‐slice ST datasets. By integrating spatial Gaussian processes with spatially hierarchical transformers, stVGP enables accurate cross‐slice alignment, robust batch effect correction, and the identification of biologically meaningful spatial domains. Critically, a key innovation of stVGP is its support for virtual tissue slices generation, allowing for continuous 3D reconstruction and interpolation of gene expression in unsampled regions. Comprehensive evaluations across diverse datasets demonstrate that stVGP consistently outperforms state‐of‐the‐art methods in alignment accuracy, domain detection, and gene expression prediction. Furthermore, stVGP enables cross‐modal generation of gene expression from histological images in human breast cancer samples, facilitating virtual transcriptomic reconstruction with high fidelity. Collectively, stVGP offers a unified, scalable framework for modeling 3D landscapes in complex tissues and developmental systems, bridging the gap between discrete 2D sections and continuous 3D biological insights. This study introduces stVGP, a variational spatial Gaussian process framework for multi-modal, multi-slice spatial transcriptomics. By integrating histological and genomic data through hybrid alignment and attention-based fusion, stVGP reconstructs coherent 3D functional landscapes. It enables virtual slice generation, cross-modal gene prediction, and niche deciphering, providing a robust computational tool for mapping complex biological architectures. ABSTRACT Spatial transcriptomics (ST) technologies are revolutionizing our ability to investigate the spatial organization of complex tissues. While ST has significantly advanced our understanding of tissue architecture, most analytical approaches remain restricted to 2D sections, limiting insights into the full 3D spatial context. Here, we introduce stVGP, a variational spatial Gaussian process framework designed to align, integrate, and reconstruct spatial coherent domains from multi-modal, multi-slice ST datasets. By integrating spatial Gaussian processes with spatially hierarchical transformers, stVGP enables accurate cross-slice alignment, robust batch effect correction, and the identification of biologically meaningful spatial domains. Critically, a key innovation of stVGP is its support for virtual tissue slices generation, allowing for continuous 3D reconstruction and interpolation of gene expression in unsampled regions. Comprehensive evaluations across diverse datasets demonstrate that stVGP consistently outperforms state-of-the-art methods in alignment accuracy, domain detection, and gene expression prediction. Furthermore, stVGP enables cross-modal generation of gene expression from histological images in human breast cancer samples, facilitating virtual transcriptomic reconstruction with high fidelity. Collectively, stVGP offers a unified, scalable framework for modeling 3D landscapes in complex tissues and developmental systems, bridging the gap between discrete 2D sections and continuous 3D biological insights. Advanced Science, EarlyView.

Enhancing Binding by Electron Transfer at Heterointerfaces of Biochar‐Modified Hydrogel to Improve Utilization Efficiency of Wastewater Recovered Nutrients

Enhancing the utilization efficiency of nutrients recovered from wastewater is achieved through hydrogel modification by biochar. The strategy improves nutrient binding to hydrogels via electron transfer at heterointerfaces, thereby reducing nutrient release rate. Consequently, biochar‐modified hydrogels facilitate vegetable growth by enhancing soil fertility and altering the microbial composition within the rhizosphere of the host. ABSTRACT Here, this work combines membrane capacitive deionization (MCDI) technology with biochar‐modified hydrogel production to recycle nutrients from wastewater efficiently. MCDI selectively recovered 76.89 ± 5.12% of ammonia and 78.94 ± 3.84% of phosphate from municipal wastewater. The biochar formed layered linear arrays within the hydrogel matrix, and enhanced hydrogen bonding led to the formation of a nanoscale hydrogel coating, creating the distinct heterointerfaces. Interestingly, biochar mediated the enhanced nutrient binding to hydrogel through electron transfer at heterointerfaces, thereby confining the nutrients in nanoscale hydrogel coating and mitigating their release rate. Therefore, the release period of nitrate, ammonia, phosphate, and potassium was prolonged by times of 0.8 to 7.3, 1 to 5.2, 0.1 to 9.1, and 4.7 to 5.7 compared to the unmodified hydrogel. The application of biochar‐modified hydrogel improved soil fertility, which in turn affected the host rhizosphere microbial composition. Furthermore, it resulted in increased lettuce fresh and dry weight compared to fertilization with nutrient‐enriched liquid and the unmodified hydrogel, respectively. This work paves the way towards sustainable nutrient utilization. Enhancing the utilization efficiency of nutrients recovered from wastewater is achieved through hydrogel modification by biochar. The strategy improves nutrient binding to hydrogels via electron transfer at heterointerfaces, thereby reducing nutrient release rate. Consequently, biochar-modified hydrogels facilitate vegetable growth by enhancing soil fertility and altering the microbial composition within the rhizosphere of the host. ABSTRACT Here, this work combines membrane capacitive deionization (MCDI) technology with biochar-modified hydrogel production to recycle nutrients from wastewater efficiently. MCDI selectively recovered 76.89 ± 5.12% of ammonia and 78.94 ± 3.84% of phosphate from municipal wastewater. The biochar formed layered linear arrays within the hydrogel matrix, and enhanced hydrogen bonding led to the formation of a nanoscale hydrogel coating, creating the distinct heterointerfaces. Interestingly, biochar mediated the enhanced nutrient binding to hydrogel through electron transfer at heterointerfaces, thereby confining the nutrients in nanoscale hydrogel coating and mitigating their release rate. Therefore, the release period of nitrate, ammonia, phosphate, and potassium was prolonged by times of 0.8 to 7.3, 1 to 5.2, 0.1 to 9.1, and 4.7 to 5.7 compared to the unmodified hydrogel. The application of biochar-modified hydrogel improved soil fertility, which in turn affected the host rhizosphere microbial composition. Furthermore, it resulted in increased lettuce fresh and dry weight compared to fertilization with nutrient-enriched liquid and the unmodified hydrogel, respectively. This work paves the way towards sustainable nutrient utilization. Advanced Science, EarlyView.

Vapor‐Assisted Catalysis Enables Precise Construction of MOF‐Derived Hierarchical Carbon Nanoarrays for High‐Performance Supercapacitors

A remote‐control strategy for catalyst design is unveiled for advanced carbon materials. During pyrolysis, zinc vapor from a physically separate source guides cobalt catalysts to construct a hierarchical carbon nanoarray. This approach prevents structural collapse while directing the dense growth of carbon nanotubes, yielding a material with exceptional performance for supercapacitors. ABSTRACT The synthesis of MOF‐derived carbons with high surface area and conductivity is challenged by a fundamental trade‐off between architectural preservation and catalytic graphitization. Here, we introduce a spatially decoupled, vapor‐assisted pyrolysis strategy where a Co‐MOF precursor array is physically separated from a vapor‐generating Zn‐MOF auxiliary. During pyrolysis, a remote Zn vapor flux simultaneously preserves the precursor's nanosheet morphology by suppressing Co nanoparticle aggregation and catalytically grows dense carbon nanotube (CNT) arrays. This process yields an integrated 0D–1D–2D hierarchical carbon architecture with high surface area and graphitization. As a self‐supporting supercapacitor electrode, the optimized material delivers a specific capacitance of 360 F g−1, excellent rate capability (53% retention at 50 A g−1), and robust cycling stability. Mechanistic studies and density functional theory calculations confirm the pivotal role of Zn vapor in modulating Co catalysis for morphology control and reveal a synergy between heteroatoms and cobalt that optimizes K+ storage kinetics. This remote‐regulation strategy establishes a generalizable platform for designing hierarchical carbon materials for advanced energy storage. A remote-control strategy for catalyst design is unveiled for advanced carbon materials. During pyrolysis, zinc vapor from a physically separate source guides cobalt catalysts to construct a hierarchical carbon nanoarray. This approach prevents structural collapse while directing the dense growth of carbon nanotubes, yielding a material with exceptional performance for supercapacitors. ABSTRACT The synthesis of MOF-derived carbons with high surface area and conductivity is challenged by a fundamental trade-off between architectural preservation and catalytic graphitization. Here, we introduce a spatially decoupled, vapor-assisted pyrolysis strategy where a Co-MOF precursor array is physically separated from a vapor-generating Zn-MOF auxiliary. During pyrolysis, a remote Zn vapor flux simultaneously preserves the precursor's nanosheet morphology by suppressing Co nanoparticle aggregation and catalytically grows dense carbon nanotube (CNT) arrays. This process yields an integrated 0D–1D–2D hierarchical carbon architecture with high surface area and graphitization. As a self-supporting supercapacitor electrode, the optimized material delivers a specific capacitance of 360 F g −1, excellent rate capability (53% retention at 50 A g −1 ), and robust cycling stability. Mechanistic studies and density functional theory calculations confirm the pivotal role of Zn vapor in modulating Co catalysis for morphology control and reveal a synergy between heteroatoms and cobalt that optimizes K + storage kinetics. This remote-regulation strategy establishes a generalizable platform for designing hierarchical carbon materials for advanced energy storage. Advanced Science, EarlyView.

Tobacco Smoke Exposure From Prenatal To Adolescent Periods Drives IBD Pathogenesis: Dynamic DNA Methylation Signatures Across Lifespan Stages

This study illustrates that maternal smoking during pregnancy (MSDP) is an independent risk factor for IBD in offspring, and DNA methylation serves as a key mechanistic pathway connecting early‐life smoking exposure with IBD risk in offspring. That highlights the urgent need for preventive interventions targeting prospective parents and minors to mitigate the rising global incidence of IBD. ABSTRACT The association between early life exposure to smoking and the risk of inflammatory bowel disease (IBD) needs to be further verified, and the potential role of DNA methylation in the association is unclear. Through an integrated study design, this study demonstrates that maternal smoking during pregnancy (MSDP) is potentially associated with increased risk of IBD, Crohn's disease (CD), and ulcerative colitis (UC) in offspring. In addition, individuals who started smoking in adolescence have a higher risk of developing CD and IBD. Mechanistically, MSDP‐associated DNA methylation alterations in ADCY7 (newborn), AKAP8L (newborn), TIGD7 (newborn), and TNF/LTA (across life stages) are significantly correlated with increased risk of CD in offspring; MSDP‐induced DNA methylation changes in PRRT1 (newborn), AHRR (across life stages), and MYO1G (across life stages) show significant associations with UC risk in offspring. Notably, the alterations of DNA methylation status within AHRR, MYO1G, and TNF/LTA loci associated with smoking exposure are present throughout the life course. Collectively, MSDP may serve as an independent risk factor for IBD in offspring, and active smoking during adolescence may cause increased risk of developing CD and IBD. MSDP may contribute to IBD susceptibility by inducing persistent DNA methylation alterations at multiple developmental stages. This study illustrates that maternal smoking during pregnancy (MSDP) is an independent risk factor for IBD in offspring, and DNA methylation serves as a key mechanistic pathway connecting early-life smoking exposure with IBD risk in offspring. That highlights the urgent need for preventive interventions targeting prospective parents and minors to mitigate the rising global incidence of IBD. ABSTRACT The association between early life exposure to smoking and the risk of inflammatory bowel disease (IBD) needs to be further verified, and the potential role of DNA methylation in the association is unclear. Through an integrated study design, this study demonstrates that maternal smoking during pregnancy (MSDP) is potentially associated with increased risk of IBD, Crohn's disease (CD), and ulcerative colitis (UC) in offspring. In addition, individuals who started smoking in adolescence have a higher risk of developing CD and IBD. Mechanistically, MSDP-associated DNA methylation alterations in ADCY7 (newborn), AKAP8L (newborn), TIGD7 (newborn), and TNF/LTA (across life stages) are significantly correlated with increased risk of CD in offspring; MSDP-induced DNA methylation changes in PRRT1 (newborn), AHRR (across life stages), and MYO1G (across life stages) show significant associations with UC risk in offspring. Notably, the alterations of DNA methylation status within AHRR, MYO1G, and TNF/LTA loci associated with smoking exposure are present throughout the life course. Collectively, MSDP may serve as an independent risk factor for IBD in offspring, and active smoking during adolescence may cause increased risk of developing CD and IBD. MSDP may contribute to IBD susceptibility by inducing persistent DNA methylation alterations at multiple developmental stages. Advanced Science, EarlyView.

Achieving Photo‐Activated Circularly Polarized Room Temperature Phosphorescence from Natural Biopolymers

This bio‐based chiral luminescent system exhibit photo‐activated CPRTP by anchoring arylboronic acids to hydroxypropyl cellulose (HPC) matrix. Notably, by controlling the drying kinetics, dynamic switchable CPRTP with opposite handedness can be obtained due to a balance of photonic bandgap (PBG) effect and chirality transfer effect induced by the HPC photonic structures. Leveraging the abundant and responsive CPRTP features, light‐controlled information storage, encryption tags, and multimode afterglow inks are well showcased. ABSTRACT Developing sustainable photo‐activated circularly polarized room temperature phosphorescent (CPRTP) materials is attractive for optoelectronic applications while are difficult to achieve. Here, we report the first example of bio‐based photo‐activated CPRTP material by anchoring arylboronic acids into hydroxypropyl cellulose (HPC) matrix via B─O covalent bonding. The rigid environment provided by B─O covalent bonds and hydrogen bonds stabilizes the triplet excitons, the residual oxygen is consumed upon continuous UV light irradiation, enabling photo‐activated CPRTP with multi‐color, high‐dissymmetry factor (glum up to ‐0.43) and prolonged lifetime from 0.22 ms to 1.57 s. More interestingly, by controlling the drying kinetics, HPC films exhibit tunable and dynamic switchable CPRTP with opposite handedness. In addition, due to the water sensitive phosphorescent nature, HPC films also show a responsive on/off CPRTP under cycled water/heat stimuli treatment. Based on the moldable and responsive CPRTP properties of the HPC based materials, the application of information photo‐controlled encrypted tags, wavelength‐dependent phosphorescent decorated patterns, multi‐mode afterglow inks have been successfully demonstrated. This study offers new insights into the intrinsic chiral luminescence of cellulose macromolecules, providing a sustainable platform for the efficient design and functional application of photo‐activated CPRTP materials. This bio-based chiral luminescent system exhibit photo-activated CPRTP by anchoring arylboronic acids to hydroxypropyl cellulose (HPC) matrix. Notably, by controlling the drying kinetics, dynamic switchable CPRTP with opposite handedness can be obtained due to a balance of photonic bandgap (PBG) effect and chirality transfer effect induced by the HPC photonic structures. Leveraging the abundant and responsive CPRTP features, light-controlled information storage, encryption tags, and multimode afterglow inks are well showcased. ABSTRACT Developing sustainable photo-activated circularly polarized room temperature phosphorescent (CPRTP) materials is attractive for optoelectronic applications while are difficult to achieve. Here, we report the first example of bio-based photo-activated CPRTP material by anchoring arylboronic acids into hydroxypropyl cellulose (HPC) matrix via B─O covalent bonding. The rigid environment provided by B─O covalent bonds and hydrogen bonds stabilizes the triplet excitons, the residual oxygen is consumed upon continuous UV light irradiation, enabling photo-activated CPRTP with multi-color, high-dissymmetry factor (g l um up to -0.43) and prolonged lifetime from 0.22 ms to 1.57 s. More interestingly, by controlling the drying kinetics, HPC films exhibit tunable and dynamic switchable CPRTP with opposite handedness. In addition, due to the water sensitive phosphorescent nature, HPC films also show a responsive on/off CPRTP under cycled water/heat stimuli treatment. Based on the moldable and responsive CPRTP properties of the HPC based materials, the application of information photo-controlled encrypted tags, wavelength-dependent phosphorescent decorated patterns, multi-mode afterglow inks have been successfully demonstrated. This study offers new insights into the intrinsic chiral luminescence of cellulose macromolecules, providing a sustainable platform for the efficient design and functional application of photo-activated CPRTP materials. Advanced Science, EarlyView.

Enhancing Interfacial Dioxygen Bridging Dynamics of Waste‐Derived Cathode Catalysts for Augmented High‐Rate Performance in Li‐O2 Batteries

This study fabricates Fine Slag/Ti4O7@TiC hybrids with interfacial dioxygen bridge coupling to optimize oxygen redox dynamics in lithium‐oxygen batteries (LOBs). Lattice distortion from oxygen vacancies and inherent charge repulsion of Ti‐O‐C interfacial coupling reconstruct and refine the surface coordination environment. LOBs using this catalyst exhibit ultralong cycle stability (210 cycles at 3000 mA g−1) and ultra‐high rate performance (1000–10 000 mA g−1). ABSTRACT Lithium–oxygen batteries (LOBs) are widely regarded as promising candidates for next‐generation high‐specific‐energy storage systems. However, their development is hindered by the disorderly accumulation of insulating products and sluggish oxygen redox kinetics (including ORR and OER). The rational design of high‐efficiency cathode catalysts is therefore critical for improving the overall performance of LOBs. In this work, a novel concept of interfacial dioxygen bridge coupling to design bifunctional cathode electrocatalysts derived from mining solid waste is introduced. Specifically, lattice distortion induced by oxygen vacancies, together with the intrinsic charge repulsion of Ti–O–C bonds on the (1–20) plane, cooperatively drives surface reconstruction and refines the local coordination environment. This structural adjustment consequently enhances the adsorption properties for ORR/OER, thereby improving the overall electrochemical performance. The Fine Slag/Ti4O7@TiC hybrid exhibits modified chemical bonding and remarkable stability at high rates. LOBs fabricated with the Fine Slag/Ti4O7@TiC catalyst deliver a reduced voltage polarization of only 1.42 V, ultralong cycle stability of 210 cycles at 3000 mA g−1, and outstanding high‐rate performance (from 1000 to 10 000 mA g−1). DFT analysis and ex‐situ characterization further elucidate the pivotal role of interfacial dioxygen bridge coupling in governing the micro‐chemical composition and manipulating the formation pathway of Li2O2. This study fabricates Fine Slag/Ti 4 O 7 @TiC hybrids with interfacial dioxygen bridge coupling to optimize oxygen redox dynamics in lithium-oxygen batteries (LOBs). Lattice distortion from oxygen vacancies and inherent charge repulsion of Ti-O-C interfacial coupling reconstruct and refine the surface coordination environment. LOBs using this catalyst exhibit ultralong cycle stability (210 cycles at 3000 mA g −1 ) and ultra-high rate performance (1000–10 000 mA g −1 ). ABSTRACT Lithium–oxygen batteries (LOBs) are widely regarded as promising candidates for next-generation high-specific-energy storage systems. However, their development is hindered by the disorderly accumulation of insulating products and sluggish oxygen redox kinetics (including ORR and OER). The rational design of high-efficiency cathode catalysts is therefore critical for improving the overall performance of LOBs. In this work, a novel concept of interfacial dioxygen bridge coupling to design bifunctional cathode electrocatalysts derived from mining solid waste is introduced. Specifically, lattice distortion induced by oxygen vacancies, together with the intrinsic charge repulsion of Ti–O–C bonds on the (1–20) plane, cooperatively drives surface reconstruction and refines the local coordination environment. This structural adjustment consequently enhances the adsorption properties for ORR/OER, thereby improving the overall electrochemical performance. The Fine Slag/Ti 4 O 7 @TiC hybrid exhibits modified chemical bonding and remarkable stability at high rates. LOBs fabricated with the Fine Slag/Ti 4 O 7 @TiC catalyst deliver a reduced voltage polarization of only 1.42 V, ultralong cycle stability of 210 cycles at 3000 mA g −1, and outstanding high-rate performance (from 1000 to 10 000 mA g −1 ). DFT analysis and ex-situ characterization further elucidate the pivotal role of interfacial dioxygen bridge coupling in governing the micro-chemical composition and manipulating the formation pathway of Li 2 O 2. Advanced Science, EarlyView.

Notch2 Directs aTreg Cell Fate toward Immunoregulation or Inflammatory Pyroptosis

Schematic illustration showing that the Notch2 intracellular domain (NICD2) facilitates pyroptosis resistance in activated Tregs through the RREB1/Foxo1 signaling pathway. In addition, Notch2‐mediated pyroptosis resistance in activated Tregs promotes immunoregulatory capacity, thereby attenuating Th2‐driven inflammatory responses in allergic rhinitis (AR). (AS1842856: Foxo1‐specific inhibitor). ABSTRACT Activated regulatory T cells (aTregs) exhibit potent immunosuppressive functions and can migrate to tissues, playing a crucial role in attenuating inflammatory responses. The precise role and molecular mechanisms through which Notch2 regulates the immunoregulatory functions of aTregs remain incompletely elucidated. Here, we elucidate the mechanisms through which Notch2 influences aTreg dynamics and mitigates allergic rhinitis (AR) development. Mechanistically, the targeted knockout of Notch2 in aTregs resulted in decreased Foxo1 expression and elevated phosphorylated ASC (p‐ASC) levels, culminating in GSDMD‐N‐mediated pyroptosis in aTregs. Moreover, the Notch2 intracellular domain (NICD2) promoted the nuclear translocation of RREB1 through direct protein–protein interactions, thereby enhancing Foxo1 transcriptional activity. Importantly, the adoptive transfer of Notch2+ aTregs significantly reduced Th2 inflammatory responses in AR mice, providing an effective therapeutic strategy for managing AR‐related inflammation. Overall, our findings establish a novel paradigm in the pathogenesis of AR in which Notch2 expression dictates the functional dichotomy of aTregs in maintaining their immunoregulatory capacity or undergoing inflammatory pyroptosis. Schematic illustration showing that the Notch2 intracellular domain (NICD2) facilitates pyroptosis resistance in activated Tregs through the RREB1/Foxo1 signaling pathway. In addition, Notch2-mediated pyroptosis resistance in activated Tregs promotes immunoregulatory capacity, thereby attenuating Th2-driven inflammatory responses in allergic rhinitis (AR). (AS1842856: Foxo1-specific inhibitor). ABSTRACT Activated regulatory T cells (aTregs) exhibit potent immunosuppressive functions and can migrate to tissues, playing a crucial role in attenuating inflammatory responses. The precise role and molecular mechanisms through which Notch2 regulates the immunoregulatory functions of aTregs remain incompletely elucidated. Here, we elucidate the mechanisms through which Notch2 influences aTreg dynamics and mitigates allergic rhinitis (AR) development. Mechanistically, the targeted knockout of Notch2 in aTregs resulted in decreased Foxo1 expression and elevated phosphorylated ASC (p-ASC) levels, culminating in GSDMD-N-mediated pyroptosis in aTregs. Moreover, the Notch2 intracellular domain (NICD2) promoted the nuclear translocation of RREB1 through direct protein–protein interactions, thereby enhancing Foxo1 transcriptional activity. Importantly, the adoptive transfer of Notch2+ aTregs significantly reduced Th2 inflammatory responses in AR mice, providing an effective therapeutic strategy for managing AR-related inflammation. Overall, our findings establish a novel paradigm in the pathogenesis of AR in which Notch2 expression dictates the functional dichotomy of aTregs in maintaining their immunoregulatory capacity or undergoing inflammatory pyroptosis. Advanced Science, EarlyView.

Unraveling Energy Flow Mechanisms in Semiconductors by Ultrafast Spectroscopy: Germanium as a Case Study

A multi‐technique pump‐probe setup capable of performing both transient reflectivity and time‐resolved Raman spectroscopy after ultrafast excitation, provides a comprehensive understanding of ultrafast electronic and phononic processes. Distinct decay rates for the temperature, frequency, and linewidth of the phonon mode in germanium are observed, along with the propagation of coherent acoustic phonon oscillations. Abstract Semiconductor materials are the foundation of modern electronics, and their functionality is dictated by the interactions between fundamental excitations occurring on (sub‐)picosecond timescales. Using time‐resolved Raman spectroscopy and transient reflectivity measurements, the ultrafast dynamics in germanium are elucidated. An increase in the optical phonon temperature is observed in the first few picoseconds, driven by the energy transfer from photoexcited holes, and the subsequent decay into acoustic phonons through anharmonic coupling. Moreover, the temperature, Raman frequency, and linewidth of this phonon mode show strikingly different decay dynamics. This difference is ascribed to the local thermal strain generated by the ultrafast excitation. Brillouin oscillations are also observed, given by a strain pulse traveling through germanium, whose damping is correlated to the optical phonon mode. These findings, supported by density functional theory and molecular dynamics simulations, provide a better understanding of the energy dissipation mechanisms in semiconductors. A multi-technique pump-probe setup capable of performing both transient reflectivity and time-resolved Raman spectroscopy after ultrafast excitation, provides a comprehensive understanding of ultrafast electronic and phononic processes. Distinct decay rates for the temperature, frequency, and linewidth of the phonon mode in germanium are observed, along with the propagation of coherent acoustic phonon oscillations. Abstract Semiconductor materials are the foundation of modern electronics, and their functionality is dictated by the interactions between fundamental excitations occurring on (sub-)picosecond timescales. Using time-resolved Raman spectroscopy and transient reflectivity measurements, the ultrafast dynamics in germanium are elucidated. An increase in the optical phonon temperature is observed in the first few picoseconds, driven by the energy transfer from photoexcited holes, and the subsequent decay into acoustic phonons through anharmonic coupling. Moreover, the temperature, Raman frequency, and linewidth of this phonon mode show strikingly different decay dynamics. This difference is ascribed to the local thermal strain generated by the ultrafast excitation. Brillouin oscillations are also observed, given by a strain pulse traveling through germanium, whose damping is correlated to the optical phonon mode. These findings, supported by density functional theory and molecular dynamics simulations, provide a better understanding of the energy dissipation mechanisms in semiconductors. Advanced Science, EarlyView.

Laterally Oriented Dendritic Passivation via In Situ Zn Reconstruction for Stabilizing NiMo Catalysts under Dynamic Electrolysis

This study highlights the effectiveness of Zn‐induced dendrite layers in enhancing the durability of NiMo HER catalysts under dynamic electrochemical conditions. Through in situ dendritic passivation, the Zn‐NiMo catalyst preserves catalytic active sites and mitigates irreversible Ni oxidation/hydroxylation during repeated load fluctuation. ABSTRACT Integrating water electrolyzers with intermittent renewable energy poses critical durability challenges from dynamic load fluctuations inducing catalyst degradation. We report a zinc‐mediated sacrificial protection strategy enhancing NiMo catalyst stability through in situ dendritic passivation. Zinc‐decorated NiMo on nickel felt (Zn‐NiMo/NF) exhibits considerable hydrogen evolution activity (94.6 mV overpotential at 50 mA cm−2) comparable to Pt/C. Under stringent load fluctuation cycling protocols (−500/50 mA cm−2), the zinc overlayer spontaneously reconstructs into laterally oriented, NiMo‐enriched dendrites providing dual protection: physical barriers suppressing dissolution (order‐of‐magnitude reductions in metal leaching) and sacrificial buffering wherein zinc preferentially oxidizes to zincate, shielding nickel from irreversible hydroxide formation. Zn‐NiMo/NF maintains stable performance while pristine NiMo/NF degrades substantially. Anion exchange membrane electrolyzer validation confirms minimal voltage escalation over 100 h cycling (1.645– 1.667 V), outperforming Pt/C (1.7028–1.857 V). This establishes sacrificial interface engineering as an effective paradigm for robust earth‐abundant electrocatalysts in renewable energy‐integrated hydrogen production. This study highlights the effectiveness of Zn-induced dendrite layers in enhancing the durability of NiMo HER catalysts under dynamic electrochemical conditions. Through in situ dendritic passivation, the Zn-NiMo catalyst preserves catalytic active sites and mitigates irreversible Ni oxidation/hydroxylation during repeated load fluctuation. ABSTRACT Integrating water electrolyzers with intermittent renewable energy poses critical durability challenges from dynamic load fluctuations inducing catalyst degradation. We report a zinc-mediated sacrificial protection strategy enhancing NiMo catalyst stability through in situ dendritic passivation. Zinc-decorated NiMo on nickel felt (Zn-NiMo/NF) exhibits considerable hydrogen evolution activity (94.6 mV overpotential at 50 mA cm −2 ) comparable to Pt/C. Under stringent load fluctuation cycling protocols (−500/50 mA cm −2 ), the zinc overlayer spontaneously reconstructs into laterally oriented, NiMo-enriched dendrites providing dual protection: physical barriers suppressing dissolution (order-of-magnitude reductions in metal leaching) and sacrificial buffering wherein zinc preferentially oxidizes to zincate, shielding nickel from irreversible hydroxide formation. Zn-NiMo/NF maintains stable performance while pristine NiMo/NF degrades substantially. Anion exchange membrane electrolyzer validation confirms minimal voltage escalation over 100 h cycling (1.645– 1.667 V), outperforming Pt/C (1.7028–1.857 V). This establishes sacrificial interface engineering as an effective paradigm for robust earth-abundant electrocatalysts in renewable energy-integrated hydrogen production. Advanced Science, EarlyView.

AXL Promotes Ischemic Myelin Repair Through Alleviating Myelin Debris Deposition and Lipid Droplets Accumulation

Microglial AXL drives white matter repair after stroke by orchestrating the cleanup of myelin debris. Mechanistically, AXL signals through EGR1 to boost Smpd1 transcription, regulating sphingolipid metabolism and preventing lipid droplet toxicity. Restoring the pathway with ASM therapy mitigates damage, positioning AXL as a key node for therapeutic intervention. ABSTRACT Ischemic white matter injury leads to long‐term neurological deficits but currently lacks effective therapies. Although AXL has been implicated in debris clearance and inflammatory regulation, its role in post‐stroke myelin repair remains unclear. Here, we report robust upregulation of microglial AXL in mice after tMCAO. Microglial AXL cKO mice exhibited worse motor and cognitive deficits up to 28 days after tMCAO, accompanied by more severe white matter damage, increased myelin debris, and greater lipid droplets (LDs) accumulation in microglia than WT controls. Longitudinal analysis showed that AXL‐deficient microglia had reduced early phagocytic capacity but increased LDs accumulation and lipid peroxidation at later stages. Transcriptomic profiling revealed altered inflammatory and sphingolipid metabolism pathways in AXL‐deficient microglia. Mechanistically, AXL regulates Smpd1 transcription via EGR1, thereby modulating sphingolipid metabolism and LDs accumulation. Remarkably, supplement with ASM (the Smpd1‐encoded enzyme) in AXL cKO mice reduced LDs accumulation and attenuated ischemic white matter injury. Collectively, these findings identify microglial AXL as an endogenous regulator of myelin repair after ischemic stroke. Microglial AXL drives white matter repair after stroke by orchestrating the cleanup of myelin debris. Mechanistically, AXL signals through EGR1 to boost Smpd1 transcription, regulating sphingolipid metabolism and preventing lipid droplet toxicity. Restoring the pathway with ASM therapy mitigates damage, positioning AXL as a key node for therapeutic intervention. ABSTRACT Ischemic white matter injury leads to long-term neurological deficits but currently lacks effective therapies. Although AXL has been implicated in debris clearance and inflammatory regulation, its role in post-stroke myelin repair remains unclear. Here, we report robust upregulation of microglial AXL in mice after tMCAO. Microglial AXL cKO mice exhibited worse motor and cognitive deficits up to 28 days after tMCAO, accompanied by more severe white matter damage, increased myelin debris, and greater lipid droplets (LDs) accumulation in microglia than WT controls. Longitudinal analysis showed that AXL-deficient microglia had reduced early phagocytic capacity but increased LDs accumulation and lipid peroxidation at later stages. Transcriptomic profiling revealed altered inflammatory and sphingolipid metabolism pathways in AXL-deficient microglia. Mechanistically, AXL regulates Smpd1 transcription via EGR1, thereby modulating sphingolipid metabolism and LDs accumulation. Remarkably, supplement with ASM (the Smpd1 -encoded enzyme) in AXL cKO mice reduced LDs accumulation and attenuated ischemic white matter injury. Collectively, these findings identify microglial AXL as an endogenous regulator of myelin repair after ischemic stroke. Advanced Science, EarlyView.

Metabolic Reprogramming Driven by Trophoblasts and Decidual XCR1+PMN‐MDSC Crosstalk Controls Adverse Outcomes Associated With Advanced Maternal Age

The interaction between trophoblasts and decidual polymorphonuclear myeloid‐derived suppressor cells (dPMN‐MDSCs) via the XCL1–XCR1 axis is crucial for fetal development during the third trimester. Disruption of this axis impairs FOXO1 activity and causes metabolic imbalance in dPMN‐MDSCs, contributing to adverse outcomes associated with advanced maternal age (AMA). ABSTRACT Trophoblast–immune cell communication is crucial during pregnancy, with impairments linked to adverse outcomes. The accumulation of decidual polymorphonuclear myeloid‐derived suppressor cells (dPMN‐MDSCs) in the third trimester is vital for fetal development. This study presents a novel crosstalk mechanism between trophoblasts and dPMN‐MDSCs that improves adverse outcomes associated with advanced maternal age (AMA). A specific dPMN‐MDSC population with high X‐C motif chemokine receptor 1 (XCR1) expression is identified, which interacts with trophoblasts through X‐C motif chemokine ligand 1 (XCL1) during the third trimester. Spontaneous fetal growth restriction observed in AMA and pregnant Xcr1−/− mice is correlated with the disruption of this interaction. Mechanistically, the deficiency in XCL1–XCR1 expression reduces nuclear FOXO1 levels, thereby impairing the transcription of FOXO1‐driven oxidative phosphorylation genes in decidual XCR1+PMN‐MDSCs. Restoring the expression of XCL1–XCR1 or FOXO1 in dPMN‐MDSCs mitigates this effect. Crucially, their adoptive transfer or treatment with XCL1/Oltipraz rescues the delayed fetal growth linked to impaired decidual XCR1+PMN‐MDSCs and metabolic imbalance. Our findings highlight the importance of trophoblast–dPMN‐MDSC communication via the XCL1–XCR1 axis, proposing metabolic reprogramming of dPMN‐MDSCs as a potential immunotherapeutic strategy for AMA‐related adverse outcomes. The interaction between trophoblasts and decidual polymorphonuclear myeloid-derived suppressor cells (dPMN-MDSCs) via the XCL1–XCR1 axis is crucial for fetal development during the third trimester. Disruption of this axis impairs FOXO1 activity and causes metabolic imbalance in dPMN-MDSCs, contributing to adverse outcomes associated with advanced maternal age (AMA). ABSTRACT Trophoblast–immune cell communication is crucial during pregnancy, with impairments linked to adverse outcomes. The accumulation of decidual polymorphonuclear myeloid-derived suppressor cells (dPMN-MDSCs) in the third trimester is vital for fetal development. This study presents a novel crosstalk mechanism between trophoblasts and dPMN-MDSCs that improves adverse outcomes associated with advanced maternal age (AMA). A specific dPMN-MDSC population with high X-C motif chemokine receptor 1 (XCR1) expression is identified, which interacts with trophoblasts through X-C motif chemokine ligand 1 (XCL1) during the third trimester. Spontaneous fetal growth restriction observed in AMA and pregnant Xcr1 −/− mice is correlated with the disruption of this interaction. Mechanistically, the deficiency in XCL1–XCR1 expression reduces nuclear FOXO1 levels, thereby impairing the transcription of FOXO1-driven oxidative phosphorylation genes in decidual XCR1 + PMN-MDSCs. Restoring the expression of XCL1–XCR1 or FOXO1 in dPMN-MDSCs mitigates this effect. Crucially, their adoptive transfer or treatment with XCL1/Oltipraz rescues the delayed fetal growth linked to impaired decidual XCR1 + PMN-MDSCs and metabolic imbalance. Our findings highlight the importance of trophoblast–dPMN-MDSC communication via the XCL1–XCR1 axis, proposing metabolic reprogramming of dPMN-MDSCs as a potential immunotherapeutic strategy for AMA-related adverse outcomes. Advanced Science, EarlyView.

HMGB2–RAD21 Axis Promotes Fibro/Adipogenic Progenitor Proliferation and Regulates Fat Infiltration

This study constructed the first developmental atlas of embryonic skeletal muscle fibro/adipogenic progenitors (FAPs) and identified an HMGB2+ FAPs subpopulation that regulates FAP pool size and muscle homeostasis. HMGB2 directly targets the RAD21 promoter, and its knockout significantly reduces FAP numbers, thereby lowering the potential for intermuscular adipocyte deposition. These findings provide novel insights into the mechanisms of fat infiltration. ABSTRACT Intermuscular fat (IMF) infiltration is not only associated with myopathies and insulin resistance, but also serves as a key determinant of meat quality in the livestock industry. However, the molecular and cellular mechanisms influencing the intermuscular adipocyte abundance remain poorly understood. Based on porcine samples, we confirmed that the differentiation of intermuscular preadipocytes begins after birth, which prompted us to focus on the changes in the number of fibro/adipogenic progenitors (FAPs) during the embryonic stage. Using single‐cell sequencing (ScRNA‐seq) analysis of pig embryonic muscle, we constructed the first developmental atlas of embryonic FAPs and identified a distinct HMGB2+ subpopulation (FAPsHMGB2+) as a key determinant of FAP pool size. When HMGB2 is knocked out, both heterozygous and homozygous mice exhibit a remarkable reduction in the number of FAPs and impaired adipogenic potential. Correspondingly, the FAPsHMGB2+ were also found during muscle regeneration in mice. Unlike targeting C/EBPβ in vitro, HMGB2 governs FAP proliferation in vivo through targeting RAD21, a gene involved in DNA replication. Collectively, these findings provide novel insights into analyzing differences in IMF content and highlight potential targets for enhancing pork quality and mitigating pathological fat infiltration in skeletal muscles. This study constructed the first developmental atlas of embryonic skeletal muscle fibro/adipogenic progenitors (FAPs) and identified an HMGB2 + FAPs subpopulation that regulates FAP pool size and muscle homeostasis. HMGB2 directly targets the RAD21 promoter, and its knockout significantly reduces FAP numbers, thereby lowering the potential for intermuscular adipocyte deposition. These findings provide novel insights into the mechanisms of fat infiltration. ABSTRACT Intermuscular fat (IMF) infiltration is not only associated with myopathies and insulin resistance, but also serves as a key determinant of meat quality in the livestock industry. However, the molecular and cellular mechanisms influencing the intermuscular adipocyte abundance remain poorly understood. Based on porcine samples, we confirmed that the differentiation of intermuscular preadipocytes begins after birth, which prompted us to focus on the changes in the number of fibro/adipogenic progenitors (FAPs) during the embryonic stage. Using single-cell sequencing (ScRNA-seq) analysis of pig embryonic muscle, we constructed the first developmental atlas of embryonic FAPs and identified a distinct HMGB2 + subpopulation (FAPs HMGB2+ ) as a key determinant of FAP pool size. When HMGB2 is knocked out, both heterozygous and homozygous mice exhibit a remarkable reduction in the number of FAPs and impaired adipogenic potential. Correspondingly, the FAPs HMGB2+ were also found during muscle regeneration in mice. Unlike targeting C/EBPβ in vitro, HMGB2 governs FAP proliferation in vivo through targeting RAD21, a gene involved in DNA replication. Collectively, these findings provide novel insights into analyzing differences in IMF content and highlight potential targets for enhancing pork quality and mitigating pathological fat infiltration in skeletal muscles. Advanced Science, EarlyView.

Targeting Peptostreptococcus anaerobius with an Iron‐Based Nanozyme Reverses Ferroptosis Resistance and Enhances Antitumor Immunity in Colorectal Cancer

An iron‐based nanozyme selectively eliminates intratumoral P. anaerobius while catalytically generating ROS to induce ferroptosis, synergistically suppressing colorectal cancer growth and activating anti‐tumor immunity through immunogenic cell death. ABSTRACT The intratumoral microbiota is a critical determinant of therapeutic outcomes in colorectal cancer (CRC). Although several microbial species have been identified that influence CRC development and treatment resistance, effective strategies for precisely modulating these bacteria remain limited. In this study, we identify Peptostreptococcus anaerobius as a tumor‐enriched anaerobe that promotes CRC progression by inhibiting ferroptosis. To counteract this, we engineered a composite iron‐based nanozyme encapsulating lincomycin, which selectively targets and eradicates intratumoral P. anaerobius, thereby reversing ferroptosis resistance in CRC. Simultaneously, the nanozyme's inherent peroxidase (POD) like activity catalyzes hydroxyl radical generation, enhancing intracellular oxidative stress and promoting ferroptosis. This dual mechanism‐microbial clearance and ROS‐mediated ferroptosis induction‐synergistically suppresses tumor growth. Moreover, ferroptotic cancer cells release large amounts of damage‐associated molecular patterns (DAMPs), which trigger immunogenic cell death (ICD), promoting dendritic cell (DC) maturation and T cell activation, thereby enhancing anti‐tumor immunity. Our findings highlight a novel ferroptosis‐centered therapeutic strategy integrating microbiota modulation and catalytic nanomedicine for precise CRC treatment. An iron-based nanozyme selectively eliminates intratumoral P. anaerobius while catalytically generating ROS to induce ferroptosis, synergistically suppressing colorectal cancer growth and activating anti-tumor immunity through immunogenic cell death. ABSTRACT The intratumoral microbiota is a critical determinant of therapeutic outcomes in colorectal cancer (CRC). Although several microbial species have been identified that influence CRC development and treatment resistance, effective strategies for precisely modulating these bacteria remain limited. In this study, we identify Peptostreptococcus anaerobius as a tumor-enriched anaerobe that promotes CRC progression by inhibiting ferroptosis. To counteract this, we engineered a composite iron-based nanozyme encapsulating lincomycin, which selectively targets and eradicates intratumoral P. anaerobius, thereby reversing ferroptosis resistance in CRC. Simultaneously, the nanozyme's inherent peroxidase (POD) like activity catalyzes hydroxyl radical generation, enhancing intracellular oxidative stress and promoting ferroptosis. This dual mechanism-microbial clearance and ROS-mediated ferroptosis induction-synergistically suppresses tumor growth. Moreover, ferroptotic cancer cells release large amounts of damage-associated molecular patterns (DAMPs), which trigger immunogenic cell death (ICD), promoting dendritic cell (DC) maturation and T cell activation, thereby enhancing anti-tumor immunity. Our findings highlight a novel ferroptosis-centered therapeutic strategy integrating microbiota modulation and catalytic nanomedicine for precise CRC treatment. Advanced Science, EarlyView.

Wide Band Gap Boron Nitride Nanodots‐Incorporated Polyetherimide Dielectrics for High‐Temperature Dielectric Energy Storage

The inherent conjugation effects between molecular chains in PEI dielectrics induce substantial energy loss escalation at elevated temperatures. This study incorporated BNNDs into PEI films, successfully achieving effective capture of motion charges under high‐temperature conditions. BNNDs effectively weaken the conjugated interactions between PEI molecular chains, thereby significantly enhancing the electrical insulation properties and energy storage capacity of PEI composite films. ABSTRACT With the ongoing trend toward miniaturization in electronic devices and the concomitant increase in power density, the operational requirements for dielectric polymer films have extended beyond conventional room‐temperature conditions. In this study, low mass fraction boron nitride nanodots (BNNDs) were incorporated into polyetherimide (PEI) films. The strong π–π interaction between BNNDs and PEI enables BNNDs to effectively intercalate between adjacent PEI molecular chains, thereby effectively weakening the interchain conjugation effects within the PEI matrix, successfully suppressing energy losses at high temperatures. Consequently, the composite film achieved an exceptional breakdown strength (Eb) of 549.4 MV m−1 at 200°C while maintaining discharge energy density (Ud) of 6.49 J cm−3 and efficiency (η) of 65%. Furthermore, the film demonstrated notable self‐healing capability following dielectric breakdown, at 200°C and 500 MV m−1, the Ud values before and after breakdown were 4.88 and 4.24 J cm−3, respectively, with η of 85% and 82%. In summary, this study demonstrates the existence of strong π‐π conjugated interactions between BNNDs and PEI molecular chains. Consequently, BNNDs can intercalate between PEI molecular chains, replacing the π–π conjugation between these chains, thereby enhancing the high‐temperature performance of aromatic dielectric polymers. The inherent conjugation effects between molecular chains in PEI dielectrics induce substantial energy loss escalation at elevated temperatures. This study incorporated BNNDs into PEI films, successfully achieving effective capture of motion charges under high-temperature conditions. BNNDs effectively weaken the conjugated interactions between PEI molecular chains, thereby significantly enhancing the electrical insulation properties and energy storage capacity of PEI composite films. ABSTRACT With the ongoing trend toward miniaturization in electronic devices and the concomitant increase in power density, the operational requirements for dielectric polymer films have extended beyond conventional room-temperature conditions. In this study, low mass fraction boron nitride nanodots (BNNDs) were incorporated into polyetherimide (PEI) films. The strong π–π interaction between BNNDs and PEI enables BNNDs to effectively intercalate between adjacent PEI molecular chains, thereby effectively weakening the interchain conjugation effects within the PEI matrix, successfully suppressing energy losses at high temperatures. Consequently, the composite film achieved an exceptional breakdown strength ( E b ) of 549.4 MV m −1 at 200°C while maintaining discharge energy density ( U d ) of 6.49 J cm −3 and efficiency (η) of 65%. Furthermore, the film demonstrated notable self-healing capability following dielectric breakdown, at 200°C and 500 MV m −1, the U d values before and after breakdown were 4.88 and 4.24 J cm −3, respectively, with η of 85% and 82%. In summary, this study demonstrates the existence of strong π-π conjugated interactions between BNNDs and PEI molecular chains. Consequently, BNNDs can intercalate between PEI molecular chains, replacing the π–π conjugation between these chains, thereby enhancing the high-temperature performance of aromatic dielectric polymers. Advanced Science, EarlyView.