Role and mechanism of mesenchymal stem cells in endometrial receptivity remodeling
Mesenchymal stem cells enhance endometrial receptivity through differentiation, angiogenesis, immunomodulation, and extracellular matrix remodeling, showing promise in treating infertility and improving pregnancy rates.
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This narrative review examines how mesenchymal stem cells (MSCs) may restore endometrial receptivity (ER) by summarizing evidence on preclinical and clinical studies across infertility contexts, including intrauterine adhesions and thin endometrium. The authors synthesize mechanisms whereby MSCs improve ER through potential differentiation into endometrial-like cells, paracrine-driven angiogenesis (e.g., VEGF), immunomodulation via induction of Treg cells and M2 macrophages, and extracellular matrix remodeling, while also noting translational barriers such as challenges in standardization and long-term safety. As part of the review, they discuss MSC source-dependent properties and identification methods (surface markers like CD73/CD90/CD105, morphology, and differentiation assays), emphasizing that culture conditions and passage number can alter cell characteristics. The paper is centrally about endometriosis? No—this review is not centrally about endometriosis or adenomyosis; it focuses on MSC mechanisms in endometrial receptivity and regeneration, with endometriosis/adenomyosis not explicitly discussed in the provided text.
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References (93)
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