Human embryonic stem cell-derived immunity-and-matrix-regulatory cells promote endometrial repair and fertility restoration in IUA rats

Early human evidence such as case series or small samples is exploring possible benefits.

• Level A · Stronger Clinical Evidence
• Level B · Emerging clinical evidence with positive signals
• Level C · Early human research exploring benefits
• Level D · Scientific groundwork from lab and animal studies
• Emerging · Emerging topic under active research

Abstract (original English)

Background Intrauterine adhesion (IUA) refers to endometrial fibrosis resulting from endometrial injury and infection. In promoting the repair of the endometrium, mesenchymal stem cells therapy has shown great potential. However, adult-derived mesenchymal stem cells (MSCs) are associated with several challenges, including invasive manipulation, susceptibility to contamination, and low proliferative capacity. Immunity-and-matrix-regulatory cells (IMRCs) derived from human embryonic stem cells exhibit enhanced immunomodulatory and anti-fibrotic capabilities. Despite their success in treating lung injury and fibrosis, membranous nephropathy, and acute liver failure, their therapeutic potential in IUA remains undetermined. Methods TGF-β1-induced human endometrial stromal cells (HESCs) were utilized to construct the IUA cell model and were treated with IMRCs conditioned medium. Morphological changes in the cells were observed, and RT-qPCR and Western blot analyses were employed to detect the expression of relevant markers during the process of epithelial-mesenchymal transition (EMT) in vitro. The IUA rat model was established using the dual injury method and subsequently treated with intrauterine infusion of IMRCs. HE and Masson staining were used to assess endometrial damage, repair and the extent of fibrosis. Fertility assays were performed to compare the effectiveness of IMRCs an

Evidence level

Early human evidence such as case series or small samples is exploring possible benefits.

Browse all related research

Filter the research library by this study's title keywords, author, or publication year.