Heart failure & cardiomyopathies
LncRNA Dilated Cardiomyopathy Repressive Transcript (DCRT) Protects Against Dilated Cardiomyopathy by Preventing NDUFS2 Alternative Splicing by Binding to PTBP1
Authors' conclusion
Our study revealed that the loss of DCRT contributed to PTBP1-mediated exon skipping of NDUFS2, thereby inducing cardiac mitochondrial dysfunction during dilated cardiomyopathy development, which could be partially treated with coenzyme Q10 supplementation.
Study context
- Population
- DCRT knockout and cardiac-specific DCRT transgenic mice, DCRT knockout cells, and myocardium of patients with dilated cardiomyopathy
Main finding
As reported in the abstract
- DCRT highly enriched in normal heart tissue; expression significantly downregulated in myocardium of patients with dilated cardiomyopathy
- DCRT-/- mice spontaneously developed cardiac dysfunction and enlargement with mitochondrial impairment
- DCRT transgene or AAV overexpression attenuated cardiac dysfunction induced by transverse aortic constriction in mice
- DCRT inhibited NDUFS2 third-exon skipping by directly binding PTBP1 in cardiomyocyte nuclei
- NDUFS2 exon skipping induced mitochondrial dysfunction by competitively inhibiting complex I activity and binding PRDX5, suppressing its antioxidant activity
- Coenzyme Q10 partially alleviated mitochondrial dysfunction in cardiomyocytes caused by DCRT reduction
Original publication
LncRNA DCRT Protects Against Dilated Cardiomyopathy by Preventing NDUFS2 Alternative Splicing by Binding to PTBP1. Circulation. Published 6 June 2024. doi:10.
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