AKT-mTOR signaling-mediated rescue of PRKAG2 R302Q mutant-induced familial hypertrophic cardiomyopathy by treatment with β-adrenergic receptor (β-AR) blocker metoprolol
Jian Zhuo, Hai-Hua Geng, Xiaohui Wu, Mengkang Fan, Hongzhuan Sheng, Jian Yao
Abstract
Background: , often shows myocardial hypertrophy and abnormal glycogen deposition in cardiomyocytes. However, it remains incurable due to a lack of a management guideline for treatment. Methods: gene, infected neonatal rat cardiomyocytes (NRCMs) and H9C2 cell lines, and then analyzed changes in AMP-activated protein kinase (AMPK) activity, cell hypertrophy, glycogen storage, and cell proliferation when presence or absence of metoprolol or protein kinase A (PKA) inhibition H89, and then analyzed the changes in AKT-mTOR signal transduction activity. Results: R302Q, including suppression of both AKT-mTOR phosphorylation and AMPK activity. Conclusions: cardiac syndrome.