The interplay between endometriosis and obesity.

Abstract

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.