ArticleAnnals of translational medicine2021
RUNX2 promotes vascular injury repair by activating miR-23a and inhibiting TGFBR2.
Article in Annals of translational medicine, 2021. 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, 7 citations in OpenAlex.
- Recent advances of miR-23 in human diseases and growth development.Non-coding RNA research · 2025Review
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundPrevious evidence has suggested that the transcription factor, runt-related transcription factor 2 (RUNX2), promotes the repair of vascular injury and activates the expression of microRNA-23a (miR-23a). TGF-β receptor type II (TGFBR2) has been found to mediate smooth muscle cells (SMCs) following arterial injury. However, the interactions among RUNX2, miR-23a and TGFBR2 in vascular injury have not been investigated thoroughly yet. Therefore, we aim to explore the mechanism of how RUNX2 triggers the expression of miR-23a and its effects on the repair of vascular injury.
methodsC57BL/6 mice were used to produce a model of arterial injury
resultsBoth RUNX2 and miR-23a exhibited low levels of expressions, while TGFBR2 had a high level of expression in mice with induced arterial injury. RUNX2 was found to bind to the promoter of miR-23a and activate miR-23a, while miR-23a targeted TGFBR2. Ectopic RUNX2 expression inhibited inflammatory cell infiltration, and promoted collagen content by upregulating miR-23a and downregulating TGFBR2. Furthermore, the overexpression of RUNX2 increased viability and decreased apoptosis in vascular smooth muscle cells (VSMCs) by activating miR-23a.
conclusionsThe overexpression of RUNX2 elevated the expression of miR-23, thus inhibiting TGFBR2 and promoting vascular injury repair.
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