ArticleCell transplantation
MALAT1/miR-7-5p/TCF4 Axis Regulating Menstrual Blood Mesenchymal Stem Cells Improve Thin Endometrium Fertility by the Wnt Signaling Pathway.
Article in Cell transplantation. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- Endometrial Repair and Regenerative Medicine: From Broad-Spectrum Regeneration to Precision Intervention.Reproductive sciences (Thousand Oaks, Calif.) · 2026Review
- LGR5 as a therapeutic target for decidualization-based endometrial mesenchymal stem cells therapy in thin endometrium.Stem cell research & therapy · 2026Article
- Molecular pathways and immune microenvironment regulation in stem cell therapy for thin endometrium: a comprehensive narrative review.Frontiers in immunology · 2026Review
- Gene regulation by non-Coding RNAs in infertility: a mechanistic review.Journal of ovarian research · 2025Review
- Long-term therapeutic effects of allogeneic mesenchymal stem cell transplantation for intrauterine adhesions.Stem cell research & therapy · 2024Article
Corrections and comments
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Authors and funding
8 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Thin endometrium (TE) is a significant factor contributing to fertility challenges, and addressing this condition remains a central challenge in reproductive medicine. Menstrual blood-derived mesenchymal stem cells (MenSCs) play a crucial role in tissue repair and regeneration, including that of TE. The Wnt signaling pathway, which is highly conserved and prevalent in eukaryotes, is essential for cell proliferation, tissue development, and reproductive functions. MALAT1 is implicated in various transcriptional and molecular functions, including cell proliferation and metastasis. However, the combined effects of the Wnt signaling pathway and the long non-coding RNA (lncRNA) MALAT1 on the regulation of MenSCs' regenerative capabilities in tissue engineering have not yet been explored. To elucidate the regulatory mechanism of MALAT1 in TE, we analyzed its expression levels in normal endometrium and TE tissues, finding that low expression of MALAT1 was associated with poor clinical prognosis. In addition, we conducted both
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