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Establishment of a Rat Model for Intrauterine Adhesions via Dual Injury: Curettage and Infection
Published on: October 3, 2025
Understanding and treating intrauterine adhesions: Insights into molecular mechanisms and innovative therapies
Dongzhi Gou1, Xiongwei Cai1, Hua He2
1Department of Obstetrics and Gynecology, Women and Children's Hospital of Chongqing Medical University, Chongqing Health Center for Women and Children, Chongqing, China.
Intrauterine adhesions (IUA) are a condition characterized by the formation of scar tissue within the uterine cavity, resulting from endometrial injury. They severely affect female fertility. Despite continuous optimization of diagnostic and therapeutic strategies, the recurrence rate remains high, indicating an incomplete understanding of the pathogenesis. This paper systematically reviews the cellular and molecular mechanisms involved in the formation of IUA as revealed by current research. It particularly emphasizes the critical roles of fibrosis-related signaling pathways, immune-inflammatory responses, angiogenesis, non-coding RNAs, epithelial-mesenchymal transition, genetic susceptibility, and mitochondrial function. Based on these molecular mechanisms, this article delves into groundbreaking approaches for both the prophylaxis and management of IUA. These strategies include modulating fibrosis signaling pathways, stem cell and exosome therapy, suppressing inflammatory responses, estrogen therapy, enhancing endometrial blood supply and angiogenesis, and platelet-rich plasma therapy. Additionally, this paper highlights the limitations of current research and discusses future research directions. It underscores the importance of integrating multi-omics research methods and developing precision medicine strategies. Thorough elucidation of the mechanism of IUA is crucial for its prevention and treatment and has important clinical significance.
Intrauterine adhesions (IUA) are a condition characterized by the formation of scar tissue within the uterine cavity, resulting from endometrial injury. They severely affect female fertility. Despite continuous optimization of diagnostic and therapeutic strategies, the recurrence rate remains high, indicating an incomplete understanding of the pathogenesis. This paper systematically reviews the cellular and molecular mechanisms involved in the formation of IUA as revealed by current research. It particularly emphasizes the critical roles of fibrosis-related signaling pathways, immune-inflammatory responses, angiogenesis, non-coding RNAs, epithelial-mesenchymal transition, genetic susceptibility, and mitochondrial function. Based on these molecular mechanisms, this article delves into groundbreaking approaches for both the prophylaxis and management of IUA. These strategies include modulating fibrosis signaling pathways, stem cell and exosome therapy, suppressing inflammatory responses, estrogen therapy, enhancing endometrial blood supply and angiogenesis, and platelet-rich plasma therapy. Additionally, this paper highlights the limitations of current research and discusses future research directions. It underscores the importance of integrating multi-omics research methods and developing precision medicine strategies. Thorough elucidation of the mechanism of IUA is crucial for its prevention and treatment and has important clinical significance.

