miR-3613-3p Is a New Diagnostic Indicator of Acute Coronary Syndrome (ACS) That Reduces Endothelial Damage by Targeting Ring Finger and CCCH-Type Domains 1 (RC3H1).

内容摘要

Focusing on acute coronary syndrome (ACS), a critical cardiovascular condition, this study explores the diagnostic utility of miR-3613-3p and its mechanistic involvement in endothelial injury. Quantitative real-time polymerase chain reaction (qRT-PCR) quantified serum and cell miR-3613-3p expression. Receiver operator characteristic (ROC) curve and logistic regression analysis assessed its diagnostic potential. Correlation analysis evaluated the association between miR-3613-3p and ACS. The effect of miR-3613-3p on hypoxia/reoxygenation (H/R)-induced human coronary artery endothelial cell (HCAEC) injury was evaluated by cell counting kit-8 (CCK-8, cell proliferation), enzyme linked immunosorbent assay (ELISA) kit (interleukin-6, IL-6; tumor necrosis factor-α, TNF-α), and commercialized assay kits (superoxide dismutase, SOD; glutathione, GSH, malonaldehyde, MDA). Dual-luciferase reporter assay validated the interaction between miR-3613-3p and ring finger and CCCH-type domains 1 (RC3H1). The recovery experiment assessed the effect of RC3H1 on H/R-induced HCAEC cell proliferation, inflammation, and oxidative stress. Compared to healthy individuals, serum miR-3613-3p in ACS, correlating with Gensini score, cardiac troponin I (cTnI), creatine kinase isoenzyme-MB (CK-MB), and left ventricular ejection fraction (LVEF), was downregulated and served as a diagnostic biomarker. In vitro, miR-3613-3p overexpression promoted cell proliferation, diminished inflammatory factor release, and reduced oxidative stress in H/R-induced HCAECs. RC3H1 was a direct target of miR-3613-3p, and its overexpression antagonized the cytoprotective influence of miR-3613-3p in H/R-induced HCAEC injury. miR-3613-3p is a novel biomarker for ACS and provides a new target for ACS intervention by alleviating endothelial damage via targeting RC3H1.