In the eye of the storm: mitochondrial damage during heart and brain ischaemia

被引：86

作者：

Borutaite, Vilmante ^{[1
]}

Toleikis, Adolfas ^{[1
]}

Brown, Guy C. ^{[2
]}

机构：

[1] Lithuanian Univ Hlth Sci, Inst Neurosci, LT-50009 Kaunas, Lithuania

[2] Univ Cambridge, Dept Biochem, Cambridge CB2 1TN, England

来源：

FEBS JOURNAL | 2013年 / 280卷 / 20期

关键词：

cell death; complexI; cytochromec; mitochondria; oxidative phosphorylation; NITRIC-OXIDE SYNTHASE; CYTOCHROME-C RELEASE; COMPLEX-I ACTIVITY; EXPERIMENTAL MYOCARDIAL-ISCHEMIA; PERMEABILITY TRANSITION PORE; TRANSIENT FOREBRAIN ISCHEMIA; FOCAL CEREBRAL-ISCHEMIA; OXIDATIVE-PHOSPHORYLATION SYSTEM; PYRUVATE-DEHYDROGENASE COMPLEX; APOPTOSIS-INDUCING FACTOR;

D O I：

10.1111/febs.12353

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

070307 [化学生物学]; 071010 [生物化学与分子生物学];

摘要：

We review research investigating mitochondrial damage during heart and brain ischaemia, focusing on the mechanisms and consequences of ischaemia-induced and/or reperfusion-induced: (a) inhibition of mitochondrial respiratory complexI; (b) release of cytochromec from mitochondria; (c) changes to mitochondrial phospholipids; and (d) nitric oxide inhibition of mitochondria. Heart ischaemia causes inhibition of cytochrome oxidase and complexI, release of cytochromec, and induction of permeability transition and hydrolysis and oxidation of mitochondrial phospholipids, but some of the mechanisms are unclear. Brain ischaemia causes inhibition of complexesI and IV, but other effects are less clear.

引用

页码：4999 / 5014

页数：16

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