Dysfunctional white adipose tissue in the progression of endometriosis: The role of the renin-angiotensin system

Obesity is a multifactorial chronic disease with pandemic-level prevalence, characterized by excessive or abnormal fat accumulation, dysregulation of body homeostasis, and chronic low-grade inflammation. This complex comorbidity shares some etiological pathways with other diseases such as endometriosis, an inflammatory and estrogen-dependent disorder that affects 5–10% women of reproductive age. The literature shows an inverse correlation between low body mass index (BMI) and the onset of endometriosis, linking obesity to more severe cases. Both endometriosis and obesity share similar underlying mechanisms, including inflammation and angiogenesis. Fat accumulation leads to overactivation of the classical renin-angiotensin system (RAS) axis, triggering impaired lipolysis and adipogenesis, increased lipogenesis, oxidative stress induction, inflammation, and insulin resistance in white adipose tissue (WAT). Although studies concerning the RAS activity of WAT in women with endometriosis are limited, the chronic inflammatory environment linked to obesity demands further investigation. This review examines the interconnections among RAS, adipogenesis, and inflammation in women with obesity and endometriosis, and their potential clinical implications.