ArticleWorld journal of stem cells2025
Bone marrow mesenchymal stem cells promote uterine healing by activating the PI3K/AKT pathway and modulating inflammation in rat models.
Article in World journal of stem cells, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
1 citing paper in PubMed.
- Differentiation of rat bone marrow mesenchymal stem cell into uterine smooth muscle cellOpen life sciences · 2026Article
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Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundUterine injury can cause uterine scarring, leading to a series of complications that threaten women's health. Uterine healing is a complex process, and there are currently no effective treatments. Although our previous studies have shown that bone marrow mesenchymal stem cells (BMSCs) promote uterine damage repair, the underlying mechanisms remain unclear. However, exploring the specific regulatory roles of BMSCs in uterine injury treatment is crucial for further understanding their functions and enhancing therapeutic efficacy.
aimTo investigate the underlying mechanism by which BMSCs promote the process of uterine healing.
methodsIn
resultsWe found that the differentially expressed genes were mainly related to cell growth, tissue repair, and angiogenesis, while the phosphoinositide 3-kinase (PI3K)/protein kinase B (AKT) pathway was highly enriched. Quantitative reverse-transcription polymerase chain reaction was used to validate differentially expressed genes, and the results demonstrated that BMSCs can upregulate genes related to regeneration and downregulate genes related to inflammation. Coculturing BMSCs promoted the migration and proliferation of USMCs, and the USMC microenvironment promoted the myogenic differentiation of BMSCs. Finally, we validated the PI3K/AKT pathway in tissues and cells and showed that BMSCs activate the PI3K/AKT pathway to promote the regeneration of uterine smooth muscle both
conclusionBMSCs upregulated uterine wound regeneration and anti-inflammatory factors and enhanced uterine smooth muscle proliferation through the PI3K/AKT pathway both
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