Abstract

The study aimed to analyze differentially expressed lncRNAs in a model of cardiac hypertrophy, specially focusing on the molecular mechanisms of lncRNA NONMMUT023529 (lncRNA N29) in myocardial hypertrophy. Based on gene microarray results, RT-qPCR validation confirmed that lncRNA N29 was significantly upregulated in TAC-induced mice cardiac tissues. Echocardiographic assessments further verified that silencing lncRNA N29 led to a marked improvement in cardiac function, which aligned with the pathological findings revealed by H&E and Masson staining. Meanwhile, immunofluorescence staining results also confirmed that silencing lncRNA N29 effectively inhibited myocardial hypertrophy. Dual luciferase reporter assay and western blot results confirmed that lncRNA can mediate miR-193b-5p/TGFBR2 axis to regulate smad/2/3 expression and mitigate the progression of myocardial hypertrophy. Our findings suggested that the close association between the protective mechanism involving in the silencing lncRNA N29 in myocardial hypertrophy and miR-193b-5p/TGFBR2 axis. We identified that lncRNA N29 might act as a therapeutic target for the treatment of myocardial hypertrophy.

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