期刊
JOURNAL OF MEMBRANE BIOLOGY
卷 209, 期 1, 页码 21-29出版社
SPRINGER
DOI: 10.1007/s00232-005-0836-6
关键词
anion channel; VSOR Cl- channel; apoptotic volume decrease; apoptosis; ischemia-reperfusion injury; anti-cancer drug
Apoptosis is an essential process in organ development, tissue homeostasis, somatic cell turnover, and the pathogenesis of degenerative diseases. Apoptotic cell death occurs in response to a variety of stimuli in physiological and pathological circumstances. Efflux of K+ and Cl- leads to apoptotic volume decrease (AVD) of the cell. Both mitochondrion-mediated intrinsic, and death receptor-mediated extrinsic, apoptotic stimuli have been reported to rapidly activate Cl- conductances in a large variety of cell types. In epithelial cells and cardiomyocytes, the AVD-inducing anion channel was recently determined to be the volume-sensitive outwardly rectifying (VSOR) Cl- channel which is usually activated by swelling under non-apoptotic conditions. Blocking the VSOR Cl- channel prevented cell death in not only epithelial and cardiac cells, but also other cell types, by inhibiting the induction of AVD and subsequent apoptotic events. Ischemia-reperfusion-induced apoptotic death in cardiomyocytes and brain neurons was also prevented by Cl- channel blockers. Furthermore, cancer cell apoptosis induced by the anti-cancer drug cisplatin was recently found to be associated with augmented activity of the VSOR Cl(-)channel and to be inhibited by a Cl- channel blocker. The apoptosis-inducing VSOR Cl- channel is distinct from ClC-3 and its molecular identity remains to be determined.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据