Cardiomyocyte-specific long noncoding RNA Trdn-as induces mitochondrial calcium overload by promoting the m6A modification of calsequestrin 2 in diabetic cardiomyopathy
Peer-Reviewed Publication
Updates every hour. Last Updated: 12-Oct-2025 08:11 ET (12-Oct-2025 12:11 GMT/UTC)
Diabetic cardiomyopathy (DCM), a major complication of diabetes mellitus, involves cardiac remodeling and dysfunction, often progressing to heart failure. Key pathological features include sarcoplasmic reticulum (SR) and mitochondrial calcium overload in cardiomyocytes, though the underlying mechanisms remain unclear. This study investigates the role of a cardiomyocyte-specific long noncoding RNA, Trdn-as, in DCM pathogenesis. Findings reveal that Trdn-as is significantly upregulated in cardiac tissues of diabetic mice and high glucose-treated cardiomyocytes. Experimental manipulation of Trdn-as in vivo and in vitro demonstrates its critical role in driving cardiac dysfunction and mitochondrial damage. Overexpression of Trdn-as in healthy mice induces DCM-like cardiac abnormalities, while silencing it in diabetic models alleviates structural and functional deficits, highlighting its potential as a therapeutic target.
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