Xu Xinyi, Li Jun, Lin He, Lin Zhe, Ji Guangcheng
College of Pharmacy, Changchun University of Chinese Medicine, Changchun, China.
School of Rehabilitation Medicine, Changchun University of Chinese Medicine, Changchun, China.
Front Immunol. 2025 Aug 12;16:1638604. doi: 10.3389/fimmu.2025.1638604. eCollection 2025.
Endometriosis is a prevalent chronic gynecological disorder. Globally, endometriosis affects approximately 5-10% of women of reproductive age, leading to symptoms such as dysmenorrhea, chronic pelvic pain, and infertility. While the precise etiology of endometriosis remains unclear, various etiological theories have been suggested to explain the condition's development. Recent research has focused on the TGF-β superfamily, which regulates cell proliferation, differentiation, migration, and immune modulation, and is increasingly recognized as a key contributor to the pathogenesis of endometriosis.
This review provides a comprehensive examination of TGF-β superfamily in endometriotic lesions. According to the recommendations of the Preferred Reporting Project for Systematic Review and Meta-Analysis (PRISMA) guidelines, a literature search was conducted in the PubMed and Web of Science database until April 30, 2025.
TGF-β superfamily contributes not only to the adhesion, invasion, and proliferation of ectopic endometrial cells but also to the mediation of fibrosis, immune modulation, and angiogenesis within endometriotic lesions. Considering the parallels between endometriosis and malignant processes, including local invasion and abnormal tissue growth, analyzing the TGF-β-mediated mechanisms offers new insights into disease progression and its oncological parallels. Exploration of TGF-β-dependent biomarkers and targeted inhibitors holds potential in advancing more effective diagnostic and therapeutic approaches.
This study emphasizes further research into TGF-β and related pathways, potentially paving the way for innovative, targeted therapeutic strategies aimed at managing endometriosis, reducing recurrence rates, and enhancing the quality of life for affected women.
子宫内膜异位症是一种常见的慢性妇科疾病。在全球范围内，子宫内膜异位症影响着约5-10%的育龄妇女，导致痛经、慢性盆腔疼痛和不孕等症状。虽然子宫内膜异位症的确切病因尚不清楚，但已提出了各种病因理论来解释该疾病的发展。最近的研究集中在转化生长因子-β（TGF-β）超家族，该家族调节细胞增殖、分化、迁移和免疫调节，并且越来越被认为是子宫内膜异位症发病机制的关键因素。
本综述全面考察了子宫内膜异位症病变中的TGF-β超家族。根据系统评价和Meta分析优先报告项目（PRISMA）指南的建议，在PubMed和Web of Science数据库中进行了文献检索，直至2025年4月30日。
TGF-β超家族不仅有助于异位子宫内膜细胞的黏附、侵袭和增殖，还参与子宫内膜异位症病变内的纤维化、免疫调节和血管生成的介导。考虑到子宫内膜异位症与恶性过程（包括局部侵袭和异常组织生长）之间的相似性，分析TGF-β介导的机制为疾病进展及其肿瘤学相似性提供了新的见解。探索TGF-β依赖性生物标志物和靶向抑制剂在推进更有效的诊断和治疗方法方面具有潜力。
本研究强调对TGF-β及相关途径进行进一步研究，这可能为旨在治疗子宫内膜异位症、降低复发率和提高受影响女性生活质量的创新靶向治疗策略铺平道路。
