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The following is a summary of “Role of fibrosis in endometriosis: a systematic review,” published in the July 2024 issue of Obstetrics & Gynecology by Vissers et al. 

Fibrosis is a key pathological feature in endometriosis, driven by myofibroblasts and TGF-β. Its role in pain development and similarities with other fibrotic diseases suggest potential non-hormonal therapies. 

Researchers conducted a retrospective study to summarize the current understanding of fibrosis in endometriosis and to identify existing knowledge gaps. 

They performed a systematic literature search in 3 biomedical databases using terms related to ‘endometriosis,’ ‘fibrosis,’ ‘myofibroblasts,’ ‘collagen,’ and ‘α-smooth muscle actin’. They included original studies on fibrosis and endometriosis, covering preclinical in vitro and animal studies and human subject research. 

The results showed 3,441 search results, with 142 studies included. Most studies had a high to moderate risk of bias. They were categorized into human observational studies, experimental studies with human-derived material, and animal studies. Observational studies detailed fibrosis histology and the co-occurrence of nerves and immune cells. In vitro studies identified pro-fibrotic pathways, while animal studies focused on therapeutic strategies targeting platelets or mast cells to reduce fibrosis. 

Investigators highlighted the central role of fibrosis and myofibroblasts in endometriosis, with platelets and TGF-β driving pro-fibrotic signaling. The close association of fibrosis with nerves suggests unique mechanisms in endometriosis, differentiating it from other fibrotic diseases. Exploring these mechanisms could lead to novel, non-hormonal therapeutic strategies for managing endometriosis-related pain. 

Source: academic.oup.com/humupd/article/30/6/706/7722011