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ABSTRACT: Background
Pathological cardiac hypertrophy is a major contributor of heart failure (HF), which seriously threatens human's health world widely. Deregulation of m6A RNA methylation, and m6A methyltransferases and de-methyltransferases have been demonstrated to act essential roles in cardiac hypertrophy and HF. Here, we studied the potential roles and its underlying mechanisms of m6A Reader YTHDF proteins in HF. In this study, we constructed HF mouse model by transverse aortic constriction surgery. Primary cardiomyocytes were isolated and stimulated with isoproterenol (ISO) or phenylephrine (PHE) to induce myocardial hypertrophy.Results
Through single-cell RNA-seq analysis, immunofluorescent staining, HE staining, Western blotting, and real time-PCR detections, we found that
SUBMITTER: Xu H
PROVIDER: S-EPMC8281596 | biostudies-literature | 2021 Jul
REPOSITORIES: biostudies-literature