Journal of Cardiovascular Pharmacology and Therapeutics · Published 2025-08-01 · DOI 10.1177/10742484251356358
Background LncRNAs are pivotal regulators in cardiovascular diseases. Sirt1-AS, a lncRNA, has been shown to play a role in cardiovascular diseases. This study aimed to explore the role of Sirt1-AS in cardiac hypertrophy and the underlying molecular mechanism. Methods A mouse model of pressure-overload cardiac hypertrophy was established via transverse aortic constriction (TAC). Cardiac tissues of TAC mice and cardiomyocytes treated with angiotensin II (AngII) were examined for Sirt1-AS and Sirt1 expression levels. The effects of Sirt1-AS overexpression or knockdown on cardiomyocyte size and hypertrophic marker expression were accessed. Furthermore, the molecular interaction between Sirt1-AS and Sirt1 were investigated. Results Sirt1-AS expression was found to be downregulated in the hearts of TAC mice and in Ang II-treated cardiomyocytes. Overexpression of Sirt1-AS attenuated cardiac hypertrophy, while its suppression exacerbated the hypertrophic response. Mechanistic studies demonstrated that Sirt1-AS directly influenced Sirt1 mRNA and protein expression levels. Moreover, the protective effects of Sirt1-AS against cardiac hypertrophy were abolished upon Sirt1 mRNA inhibition. Conclusion Our findings suggest that Sirt1-AS exerts a protective effect against cardiac hypertrophy by modulating Sirt1 expression. This research provides novel insights into the role of lncRNAs in cardiac hypertrophy and highlights Sirt1-AS as a potential therapeutic target for the treatment of cardiac hypertrophy.
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