ArticleJournal of cardiothoracic surgery2026
LncRNA GAS6-AS1 affects doxorubicin‑induced cardiomyocyte injury in H9c2 cells by regulating miR‑152‑3p: a cellular model relevant to heart failure.
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
objectiveTo explore the diagnostic significance of LncRNA GAS6-AS1 in chronic heart failure (CHF) and its molecular mechanism of influencing cardiomyocyte function through the regulation of miR-152-3p.
methodsThis study incorporated 126 patients diagnosed with CHF and 124 healthy control subjects. The serum level of GAS6-AS1 was determined via RT-qPCR, and its diagnostic efficacy was assessed through ROC curve. A cell injury model was established by stimulating H9c2 cells with DOX. CCK-8, flow cytometry and RT-qPCR were used to analyze the effects of these on cell viability, apoptosis and inflammatory factors (TNF-α, IL-6, IL-1β). The targeting relationship between GAS6-AS1 and miR-152-3p was verified by DLR.
resultsThe expression of GAS6-AS1 in the serum of CHF patients was significantly downregulated. ROC analysis showed that the sensitivity of GAS6-AS1 in the diagnosis of CHF was 84.90%, the specificity was 77.40%, and the AUC was 0.888 (95% CI: 0.849-0.928). Overexpression of GAS6-AS1 could mitigate the reduction in cell viability and the elevation in apoptosis induced by DOX in H9c2 cells, and inhibit the expression of pro-inflammatory factors. GAS6-AS1 could directly bind to miR-152-3p. Overexpression of miR-152-3p could reverse the inhibitory effect of GAS6-AS1 on cell apoptosis and the release of inflammatory factors.
conclusionGAS6-AS1 can act as a potential diagnostic biomarker for CHF. It might accomplish this by targeting and suppressing miR-152-3p, thus decreasing cardiomyocyte apoptosis and inflammatory reactions.
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