Key result
Elevated miR-193a-3p linked to ~3.2-fold higher risk of cerebral ischemic events in carotid stenosis.
Why the study?
Does elevated serum miR-193a-3p expression diagnose carotid artery stenosis and predict cerebral ischemic events in patients with carotid artery stenosis?
Cohort (n=192)
No
Does elevated serum miR-193a-3p expression diagnose carotid artery stenosis and predict cerebral ischemic events in patients with carotid artery stenosis?
Answers are grounded in this paper and cite their sources.
Serum miR-193a-3p is a promising diagnostic and prognostic biomarker for carotid artery stenosis severity and future cerebral ischemic events, acting mechanistically by targeting LAMC1 to promote vascular smooth muscle cell injury and phenotypic switching.
Given the numerous advantages of microRNAs as biomarkers in diseases, this study investigated the role of miR-193a-3p in carotid artery stenosis (CAS), aiming to provide novel biomarkers for CAS clinical management. RT-qPCR measured serum miR‑193a‑3p expression in 107 CAS subjects and 85 healthy individuals. The diagnostic and prognostic potential of miR-193a-3p in CAS was evaluated by ROC curve, logistic regression analysis, Kaplan‑Meier and COX regression analysis. The involvement of miR-193a-3p in ox-LDL-induced human vascular smooth muscle cells (hVSMCs) was evaluated through cell counting kit-8, transwell, enzyme-linked immunosorbent assay kits and phenotype switching markers. Bioinformatics and dual‑luciferase reporter assay validated downstream targets. Rescue experiments assessed the effect of miR-193a-3p/LAMC1 axis-mediated regulation in ox-LDL-induced hVSMCs. Upregulated miR‑193a‑3p expression was observed in CAS group and distinguished CAS from healthy individuals (AUC = 0.839) and differentiated stenosis severity (mild vs. moderate: AUC = 0.822; mild vs. severe: AUC = 0.895). High miR‑193a‑3p expression predicted the occurrence of cerebral ischemic events (CIEs) among subjects with CAS. In vitro, miR‑193a‑3p inhibition reduced cell proliferation, migration, inflammation (decreased IL-6 and TNF-α) and oxidative stress (diminished MDA, enhanced SOD), and reversed phenotype switching (upregulated α-SMA, downregulated osteopontin) in ox‑LDL‑induced hVSMCs. LAMC1 was confirmed as the target, and the above effects of miR‑193a‑3p suppression were counteracted by silencing LAMC1. Upregulated miR-193a-3p expression in CAS showed diagnostic and prognostic potential for CAS. In vitro, miR-193a-3p regulated the cell injury and phenotype switch through targeting LAMC1 in ox-LDL-stimulated hVSMCs, suggesting a novel insight for CAS clinical treatment.
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Liu et al. (2026) conducted a cohort in Carotid artery stenosis (CAS) (n=192). High serum miR-193a-3p expression vs. Low serum miR-193a-3p expression (and healthy controls for diagnostic comparison) was evaluated on Occurrence of cerebral ischemic events (CIEs) among patients with carotid artery stenosis over a median 60-month follow-up (HR 3.217, 95% CI 1.246-8.304, p=0.016). High serum miR-193a-3p expression independently predicted cerebral ischemic events in carotid artery stenosis patients and distinguished CAS from controls.
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