ArticleJournal of molecular histology2026
miR-567 indicates atherosclerosis development and regulates inflammation, phenotype switch, proliferation, and migration of platelet-derived growth factor (PDGF)-BB-induced vascular smooth muscle cells (VSMCs) via CSF1R.
Article in Journal of molecular histology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
This study evaluated the clinical significance of miR-567 in atherosclerosis and its regulatory effect on PDGF-BB-induced VSMCs, aiming to identify a novel biomarker for the risk and progression of atherosclerosis. The study enrolled 113 atherosclerosis patients and 126 non-atherosclerosis patients. Serum miR-567 level was compared between the two groups and its significance in disease severity was assessed. T/G human VSMC was induced with PDGF-BB, and based on this cell model, the regulatory effect and potential mechanism of miR-567 was estimated. miR-567 was upregulated in atherosclerosis patients and showed diagnostic significance (AUC = 0.875). miR-567 was positively correlated with homocysteine, total cholesterol, and low-density lipoprotein, and negatively correlated with high-density lipoprotein (r > 0.7, P < 0.0001). miR-567 was upregulated in PDGF-BB-induced VSMCs, and silencing miR-567 showed protective effect on PDGF-BB-induced VSMCs. CSF1R was negatively correlated with miR-567. Silencing CSF1R reversed the protective effect of miR-567 silencing on PDGF-BB-induced VSMCs.
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