Endometriosis: Cellular and Molecular Mechanisms Leading to Fibrosis

Endometriosis is a chronic inflammatory condition affecting women of reproductive age. A relevant feature of endometriosis is the presence of fibrotic tissue inside and around the lesions, thus contributing to the classic endometriosis-related symptoms, pain, and infertility. The molecular mechanisms responsible for the development of fibrosis in endometriosis are not yet defined. The present review aimed to examine the biological mechanisms and signalling pathways involved in fibrogenesis of endometriotic lesions, highlighting the difference between deep infiltrating and ovarian endometriosis. The main cell types involved in the development of fibrosis are platelets, myofibroblasts, macrophages, and sensory nerve fibers. Members of the transforming growth factor (TGF) -beta family, as well as the receptor Notch, or the bioactive sphingolipid sphingosine 1-phosphate (S1P), play a role in the development of tissue fibrosis, resulting in their metabolism and/or their signalling pathways altered in endometriotic lesions. It is relevant the knowledge of the molecular mechanisms that guide and support fibrosis in endometriosis, to identify new drug targets and provide new therapeutic approaches to patients.

Automated summary

Endometriosis, a chronic inflammation in women of reproductive age, is characterized by the presence of fibrotic tissue inside and around lesions. The development of fibrosis is influenced by various cell types and molecular mechanisms, such as platelets, myofibroblasts, macrophages, and sensory nerve fibers, as well as the involvement of transforming growth factor-beta, Notch receptor, and sphingosine 1-phosphate (S1P). Understanding these molecular mechanisms is important for identifying new drug targets and developing novel therapeutic approaches for endometriosis patients.