Journal of International Reproductive Health/Family Planning ›› 2025, Vol. 44 ›› Issue (5): 429-433.doi: 10.12280/gjszjk.20250122

• Review • Previous Articles     Next Articles

Research Progress on Galectin-3 in the Pathogenesis of Endometriosis

ZHOU Yuan, WANG Zhen-zhen, CAO Meng-dong, SHEN Xue()   

  1. Department of Obstetrics and Gynecology, Postgraduate Union Training Base of Xiangyang No.1 People′s Hospital, School of Medicine, Wuhan University of Science and Technology, Xiangyang 441000, Hubei Province, China (ZHOU Yuan, CAO Meng-dong); Department of Obstetrics and Gynecology, Xiangyang No.1 People′s Hospital, Hubei University of Medicine, Xiangyang 441000, Hubei Province, China (WANG Zhen-zhen, SHEN Xue)
  • Received:2025-03-17 Published:2025-09-15 Online:2025-09-12
  • Contact: SHEN Xue E-mail:FKxy1025@163.com

Abstract:

The pathogenesis of endometriosis (EMs), as a common and difficult gynecological disease, is not very clear. The possible mechanisms include chronic inflammation, neovascularization, estrogen dependence, weakened progesterone response, epithelial-mesenchymal transition and fibrosis, etc. Galectin-3 is the only member of the Galectinin family with a chimeric structure. It participates in mutiple biological processes such as cell adhesion, migration, invasion, angiogenesis and fibrosis, which is closely related to the occurrence of cancer and inflammatory diseases. The correlation between Galectin-3 and EMs has received the extensive attention in recent years. The latest studies have shown that the overexpression of Galectin-3 can affect the occurrence and development of EMs by promoting the survival of inflammatory cells, epithelial-mesenchymal transition, fibrosis, and participating in the regulation of sex hormones. This article summarizes the functions of Galectin-3 and its correlation with the pathophysiology of EMs, with the aim of providing new ideas for the clinical diagnosis and treatment of EMs.

Key words: Endometriosis, Galectin 3, Inflammation, Epithelial-mesenchymal transition, Neovascularization, pathologic, Fibrosis, Gonadal steroid hormones