ArticleFrontiers in cardiovascular medicine2025
Bone marrow mesenchymal stem cell-derived exosomal microRNA-335 alleviates vascular calcification by targeting SP1.
Article in Frontiers in cardiovascular medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 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
3 citing papers in PubMed.
- Review
- PTGIS inhibited osteogenic and promoted angiogenic differentiation of bone marrow mesenchymal stem cells via endoplasmic reticulum stress mediated PI3K/AKT signaling.Stem cell research & therapy · 2026Article
- Review
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Authors and funding
8 authors.
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Abstract
Background: Vascular calcification (VC) is a critical pathological characteristic of cardiovascular diseases like atherosclerosis, frequently linked to phenotypic alterations in vascular smooth muscle cells (VSMCs) and the activation of bone-forming genes. Exosomes derived from bone marrow mesenchymal stem cells (BMSCs) have been shown to significantly attenuate VSMC calcification. Methods: To investigate whether BMSC-derived exosomes mitigate VSMC calcification through microRNAs (miRNAs) regulation, we developed an Results: Functional and phenotypic assessments revealed that BMSC-derived exosomes markedly reduced VSMC calcification. RT-qPCR analysis further indicated that BMSC-derived exosomes regulate VSMC calcification by modulating rno-miR-335 (miR-335). The miR-335 mimic notably suppressed the expression of the osteogenic regulator RUNX2 in VSMCs. Dual-luciferase reporter assays demonstrated that SP1 is a direct target of miR-335. Exosomal miR-335 inhibited SP1 expression, resulting in reduced mRNA and protein levels of RUNX2. Conclusion: This study highlights that BMSC-derived exosomes regulate VC via the miR-335/SP1 axis, offering novel molecular targets for treating VC.
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