MicroRNA-22 Regulates Cardiac Hypertrophy and Remodeling in Response to Stress

• DOI: 10.1161/circresaha.112.300682
• Publication Date: 2013-03-23T05:33:09Z
• Authors: Zhan-Peng Huang; Jinghai Chen; Hee Young Seok; Zheng Zhang; Masaharu Kataoka; Xiaoyun Hu; Da-Zhi Wang
• Keywords: Cardiac myocyte

The adult heart is composed primarily of terminally differentiated, mature cardiomyocytes that express signature genes related to contraction. In response mechanical or pathological stress, the undergoes hypertrophic growth, a process defined as an increase in cardiomyocyte cell size without number. However, molecular mechanism cardiac hypertrophy not fully understood.To identify and characterize microRNAs regulate remodeling.Screening for muscle-expressed are dynamically regulated during muscle differentiation identified microRNA-22 (miR-22) cardiac- skeletal muscle-enriched microRNA upregulated myocyte hypertrophy. Overexpression miR-22 was sufficient induce We generated mouse models with global cardiac-specific deletion, we found essential growth stress. miR-22-null hearts blunted remodeling 2 independent stressors: isoproterenol infusion activated calcineurin transgene. Loss sensitized mice development dilated cardiomyopathy under stress conditions. Sirt1 Hdac4 targets heart.Our studies uncover critical regulator remodeling.