The interplay between endometriosis and obesity

Endometriosis, characterized by uterine-like tissue growth outside the uterus, is a complex disorder with significant clinical implications. This review explores how body composition – both low body mass index (BMI) and obesity – modulates endometriosis progression through metabolic, hormonal, and immune-inflammatory pathways. Obesity-driven leptin signaling emerges as a pivotal link, promoting systemic inflammation, angiogenesis, and lesion persistence via Janus kinase–signal transducer and activator of transcription (JAK–STAT) pathways. Shared molecular mechanisms between endometriosis and obesity highlight opportunities for precision medicine and targeted therapies. By addressing leptin-driven pathways and metabolic dysfunction, we introduce innovative strategies, offering novel insights into the improved management of this multifaceted condition.