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Updated: Sep 19, 2026
A Doxorubicin-Induced Murine Model of Dilated Cardiomyopathy In Vivo
Published on: May 16, 2020
LncRNA GAS6-AS1 affects doxorubicin‑induced cardiomyocyte injury in H9c2 cells by regulating miR‑152‑3p: a cellular
1Department of Cardiology, Xiantao Hospital of Traditional Chinese Medicine Affiliated to Hubei University of Chinese Medicine (Xiantao Hospital of Traditional Chinese Medicine), Xiantao, 433000, China.
Objective:
To 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.
Methods:
This 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.
Results:
The 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.
Conclusion:
GAS6-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.
