期刊
ADVANCED DRUG DELIVERY REVIEWS
卷 60, 期 13-14, 页码 1471-1477出版社
ELSEVIER
DOI: 10.1016/j.addr.2008.03.020
关键词
Anoxia; Oxygen glucose deprivation; Ischemia; Brain; Mitochondria; ATP-sensitive potassium channels; Excitotoxicity; Necrosis; Apoptosis
资金
- NIH [HL-077731, HL-030260, HL-065380]
- Y. F Wu Research and Education Fund
- WFUSM Venture Fund
- K.G Phillips Fund for the Prevention and Treatment of Heart Disease WFUSM Interim Funding
- Hungarian Science Foundation [K 68976, K 63401, IN 69967]
- NATIONAL HEART, LUNG, AND BLOOD INSTITUTE [T32HL007731, R01HL030260, R01HL065380, R01HL077731] Funding Source: NIH RePORTER
Preconditioning represents the condition where transient exposure of cells to an initiating event leads to protection against subsequent, potentially lethal stimuli. Recent studies have established that mitochondrial-centered mechanisms are important mediators in promoting development of the preconditioning response. However, many details concerning these mechanisms are unclear. The purpose of this review is to describe the initiating and subsequent intracellular events involving mitochondria which can lead to neuronal preconditioning. These mitochondrial specific targets include: I) potassium channels located on the inner mitochondrial membrane; 2) respiratory chain enzymes; and 3) oxidative phosphorylation. Following activation of mitochondrial ATP-sensitive potassium (mitoK(ATP)) channels and/or increased production of reactive oxygen species (ROS) resulting from the disruption of the respiratory chain or during energy substrate deprivation. morphological changes or signaling events involving protein kinases confer immediate or delayed preconditioning on neurons that will allow them to survive otherwise lethal insults. While the mechanisms involved are not known with certainty, the results of preconditioning are the enhanced neuronal viability, the attenuated influx of intracellular calcium, the reduced availability of ROS, the Suppression of apoptosis, and the maintenance of ATP levels during and following stress. (C) 2008 Elsevier B.V. All rights reserved.
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