Regression of cardiac hypertrophy by cyclic guanosine monophosphate-dependent protein kinase signaling are myocytes active sources or mere beneficiaries?
Regression of cardiac hypertrophy by cyclic guanosine monophosphate-dependent protein kinase signaling are myocytes active sources or mere beneficiaries?
复制标题
通过环鸟苷单磷酸依赖性蛋白激酶信号传导来消退心脏肥大是心肌细胞的活性来源还是仅仅是受益者？
DOI：
10.1016/j.jacc.2010.09.005
复制
发表时间：
2010
影响因子：
24
通讯作者：
Akar,FadiG
中科院分区：
文献类型：
--
作者：
Hajjar,RogerJ;Akar,FadiG
左心室肥大（LVH）响应升高的全身压力形成一种适应性机制，使心脏能够在面对外部压力时维持心输出量。然而，由于肥厚与复杂的电生理、结构、分子、机械和代谢重塑相关 (1, 2)，因此它最终成为心力衰竭、心律失常和心源性猝死的主要危险因素。
Left ventricular hypertrophy (LVH) in response to elevated systemic pressure forms an adaptive mechanism that allows the heart to maintain cardiac output in the face of external stress. However, because hypertrophy is associated with complex electrophysiological, structural, molecular, mechanical, and metabolic remodeling (1, 2), it ultimately becomes a leading risk factor for heart failure, arrhythmias, and sudden cardiac death.