Rahman Md Saidur, Park Yunjeong, Hosseinirad Hossein, Shin Jung-Ho, Jeong Jae-Wook
Department of Obstetrics, Gynecology, and Women's Health, University of Missouri School of Medicine, Columbia, MO 65211, USA.
Department of Obstetrics and Gynecology, Guro Hospital, Korea University Medical Center, Seoul 02841, Republic of Korea.
Trends Endocrinol Metab. 2025 Apr 24. doi: 10.1016/j.tem.2025.03.011.
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.
子宫内膜异位症的特征是子宫外出现类似子宫内膜的组织生长，是一种具有重大临床意义的复杂疾病。本综述探讨了身体组成——低体重指数（BMI）和肥胖——如何通过代谢、激素和免疫炎症途径调节子宫内膜异位症的进展。肥胖驱动的瘦素信号传导成为一个关键环节，通过 Janus 激酶-信号转导子和转录激活子（JAK-STAT）途径促进全身炎症、血管生成和病灶持续存在。子宫内膜异位症和肥胖之间共享的分子机制凸显了精准医学和靶向治疗的机会。通过解决瘦素驱动的途径和代谢功能障碍，我们引入了创新策略，为改善这种多方面疾病的管理提供了新的见解。
