摘要
位于心肌线粒体内膜上的解耦联蛋白 (UCPs) ,作为质子通道驱散氧化呼吸时形成的H+梯度 ,使产能转化为产热 ,从而增加呼吸 ,阻止ATP形成 ,并抑制活性氧族的产生 ,最终阻止了心肌细胞的程序性死亡。脂肪酸、寒冷、甲状腺激素、肾上腺素等能调控UCPs的浓度和活性。UCPs在心力衰竭中的作用仍然不清楚 。
As a proton channel in the inner mitochondrial membrane, the uncoupling proteins (UCPs) disperse the H + gradient and increase the thermogenic action. So they increase respiration, decrease ATP production, prevent reactive oxygen species formation and resulting apoptosis. Fatty acid metabolism, coldness, thyroid hormones and adrenal hormones control the UCPs expression in cardiac myocyte. At present, the roles of UCPs in heart failure are not completely resolved and some are still hypothetical.
出处
《医学研究生学报》
CAS
2002年第4期358-360,共3页
Journal of Medical Postgraduates
关键词
解耦联蛋白
线粒体
心肌细胞
心力衰竭
Uncoupling proteins
Mitochondrion
Cardiac myocyte
Heart failure
