Cell Death and Heart Failure in Obesity: Role of Uncoupling Proteins.
Cell Death and Heart Failure in Obesity: Role of Uncoupling Proteins.
复制标题
肥胖的细胞死亡和心力衰竭：解偶联蛋白的作用。
DOI：
10.1155/2016/9340654
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发表时间：
2016
影响因子：
--
通讯作者：
El-Hafidi M
中科院分区：
文献类型：
--
作者：
Ruiz-Ramírez A;López-Acosta O;Barrios-Maya MA;El-Hafidi M
Metabolic diseases such as obesity, metabolic syndrome, and type II diabetes are often characterized by increased reactive oxygen species (ROS) generation in mitochondrial respiratory complexes, associated with fat accumulation in cardiomyocytes, skeletal muscle, and hepatocytes. Several rodents studies showed that lipid accumulation in cardiac myocytes produces lipotoxicity that causes apoptosis and leads to heart failure, a dynamic pathological process. Meanwhile, several tissues including cardiac tissue develop an adaptive mechanism against oxidative stress and lipotoxicity by overexpressing uncoupling proteins (UCPs), specific mitochondrial membrane proteins. In heart from rodent and human with obesity, UCP2 and UCP3 may protect cardiomyocytes from death and from a state progressing to heart failure by downregulating programmed cell death. UCP activation may affect cytochrome c and proapoptotic protein release from mitochondria by reducing ROS generation and apoptotic cell death. Therefore the aim of this review is to discuss recent findings regarding the role that UCPs play in cardiomyocyte survival by protecting against ROS generation and maintaining bioenergetic metabolism homeostasis to promote heart protection.
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