摘要
心肌细胞钙离子失去稳态调节是多种心脏病变的基础,与缺血/再灌注损伤关系密切。缺血/再灌注引起细胞内外钙离子调节方式发生变化,导致胞浆及线粒体基质钙超载;通过能量依赖性肌纤维过度收缩、钙蛋白酶介导的细胞蛋白水解、线粒体渗透性转换孔的开放、诱导细胞凋亡,以及关闭缝隙连接通道使细胞活动失同步等途径致使心肌结构破坏、功能下降或电生理紊乱。干预细胞钙离子调节不同的环节,纠正或维持钙离子稳态则被证实有助于防止或减轻心肌缺血/再灌注损伤。
The loss of homeostasis regulation of calcium ion (Ca^2+)in myocardium is the pathological basis of many heart diseases and it is closely related to myocardial ischemia-reperfusion injury.Altered Ca^2+ regulation in and out of cells induced by ischemia-reperfusion lead to calcium overload in cytoplasm and mitochondrial matrix.Cell damage,dysfunction or electrophysiological disorder occur as a resuh of energy-dependent hypercontraction of myocardial fibers,calpain-mediate hydrolysis of cell proteins, opening of mitochondrial permeability transition pores,apoptosis and uncoupling cell activation related to closed gap junctions.Modulation of different steps of the Ca^2+ cycle,correcting or maintaining calcium homeostasis,has been proven to be helpful for prevention or mitigation of myocardial ischemia-reperfusion injury.
作者
肖滨
黄小波
XIAO Bin;HUANG Xiao-bo(Department of Traditional Chinese Medicine,Xuanwu Hospital,Capital Medical University,Beijing 100053, China)
出处
《心脏杂志》
CAS
2019年第1期98-102,共5页
Chinese Heart Journal
基金
北京市中西医结合老年疾病专项基金资助(2012-191)
关键词
钙离子
稳态
钙超载
钙蛋白酶
线粒体渗透性转换孔
心肌
缺血/再灌注损伤
calcium
homeostasis
calcium overload
calpain
mitochondrial permeability transition pore
myocardium
ischemic reperfusion injury
