摘要
心力衰竭被认为是一种心肌代谢性疾病,而解偶联蛋白-2是参与心肌生物能量代谢及功能调节的重要分子。解偶联蛋白-2是位于线粒体内膜的一类载体蛋白,能将内膜外H+运回到线粒体基质,导致氧化磷酸化脱偶联。解偶联蛋白-2的轻微脱偶联作用能减少线粒体活性氧生成而发挥细胞保护作用,然而,这种轻微脱偶联作用也将导致心肌细胞生物能量代谢、Ca2+内环境稳定、兴奋-收缩偶联异常,有可能进一步加重心力衰竭及诱发各种心律失常的发生。因此,进一步认清解偶联蛋白-2在心脏的功能作用,适当调节解偶联蛋白-2的表达将有助于临床心力衰竭的治疗。
Heart failure is considered to be a myocardial metabolic disease, and uncoupling protein 2 (UCP2) is a important molecule which involved in biological energy metabolism and regulating myocardial functions. UCP2 is one kind of carrier proteins located in the mitochondrial inner membrane, and can transmit H^+ from intermembrane space to the mitochondria matrix, that will result in oxidative phosphorylation uncoupling. UCP2 play a critical role of cell protection through reducing reactive oxygen species ( ROS), however, mildly uncoupling effect also resulted in abnormal of myocardial cell biological energy metabolism, Ca^2+ homeostasis and excited-shrinkage coupling, which could further aggravate heart failure and induce various arrhythmia. As a result, it could contribute to the therapy of cardiac failure that further recognizing the role of UCP2 in heart and reasonably regulating the expression of UCP2.
出处
《心血管病学进展》
CAS
2013年第2期257-260,共4页
Advances in Cardiovascular Diseases
基金
国家自然基金(项目批准号:31140019)资助