ArticleJournal of cardiothoracic surgery2026
miR-330-3p promotes acute coronary syndrome progression via targeting RGS5.
Article in Journal of cardiothoracic surgery, 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
backgroundAcute coronary syndrome (ACS), a lethal cardiovascular emergency, urgently requires novel biomarkers for early diagnosis. While miR-330-3p is dysregulated in cardiovascular diseases, its specific role in ACS pathogenesis remains undefined.
methodsClinical data and serum were collected from 110 ACS patients and 110 healthy controls. MiR-330-3p expression was quantified by qRT-PCR and correlated with clinical indicators using Pearson analysis. The diagnostic utility was determined by ROC analysis; ACS risk factors were identified via logistic regression. The ENCORI database was used to predict miR-330-3p targets, validated through dual luciferase reporter assays. In vitro, the effects of miR-330-3p and RGS5 on endothelial function (proliferation by CCK-8, apoptosis by flow cytometry, inflammation by ELISA) were assessed in ox-LDL-stimulated human aortic endothelial cells (HAECs).
resultsUpregulation of serum miR-330-3p in ACS patients was positively associated with WBC, NEUT, CK-MB, and NT-proBNP levels. MiR-330-3p demonstrated strong diagnostic accuracy for ACS and served as an independent risk factor. Dual luciferase assays verified the direct binding relationship between miR-330-3p and RGS5. In ox-LDL-treated HAECs, inhibiting miR-330-3p expression promoted cell proliferation, inhibited apoptosis, and suppressed inflammatory factor release, while knocking down RGS5 reversed these effects.
conclusionUpregulated miR-330-3p in ACS demonstrates diagnostic value and correlates with disease severity. MiR-330-3p promotes ACS progression by targeting RGS5, inducing endothelial dysfunction and inflammation.
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