4.5 Review

Endometriosis: Cellular and Molecular Mechanisms Leading to Fibrosis

期刊

REPRODUCTIVE SCIENCES
卷 30, 期 5, 页码 1453-1461

出版社

SPRINGER HEIDELBERG
DOI: 10.1007/s43032-022-01083-x

关键词

Endometriosis; Endometrioma; Deep infiltrating endometriosis; Fibrosis; TGF-beta; S1P

向作者/读者索取更多资源

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.
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.

作者

我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。

评论

主要评分

4.5
评分不足

次要评分

新颖性
-
重要性
-
科学严谨性
-
评价这篇论文

推荐

暂无数据
暂无数据