ArticleStem cell reports2025
A novel miRNA-TF-mRNA regulatory network associated with cellular senescence in osteoporosis.
Article in Stem cell reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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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
2 citing papers in PubMed.
- Article
- Endothelial EPAS1 as a prognostic and therapeutic target in acute myocardial infarction: integrative bioinformatics, Mendelian randomization and experimental validation.Frontiers in pharmacology · 2026Article
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Authors and funding
4 authors.
Funding
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Abstract
This study investigated the role of miR-22-3p/ESR1 axis in osteoporosis (OP) pathogenesis. Bioinformatics analysis of OP datasets and patient bone marrow samples revealed significant upregulation of miR-22-3p accompanied by downregulation of ESR1. Mechanistic validation via dual-luciferase reporter assays, RNA pull-down, and molecular docking confirmed that miR-22-3p directly targets and suppresses ESR1 expression. Functional in vitro assays in human bone marrow mesenchymal stem cells (hBMSCs) demonstrated that miR-22-3p overexpression accelerated both cellular senescence (CS) and adipogenic differentiation. Notably, this effect was reversed by ESR1 overexpression. In an aged mouse model, local intra-bone marrow administration of a miR-22-3p inhibitor effectively reduced bone marrow mesenchymal stem cell (BMSC) senescence, improved bone microstructure, and attenuated OP progression. These findings establish that the miR-22-3p-ESR1 regulatory axis critically drives OP development by coordinately promoting CS and adipogenic differentiation while suppressing osteogenesis. This pathway provides a promising mechanistic foundation for future therapeutic strategies targeting OP.
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Registered trials
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