期刊
CELL METABOLISM
卷 23, 期 2, 页码 254-263出版社
CELL PRESS
DOI: 10.1016/j.cmet.2015.12.009
关键词
-
资金
- Medical Research Council (UK)
- British Heart Foundation
- Human Frontiers Science Program fellowship
- MRC [G1100562, MC_UU_12022/6, MC_U105663142] Funding Source: UKRI
- Medical Research Council [MC_UU_12022/6, MC_U105663142, G1100562] Funding Source: researchfish
Ischemia-reperfusion (IR) injury occurs when blood supply to an organ is disrupted-ischemia-and then restored-reperfusion-leading to a burst of reactive oxygen species (ROS) from mitochondria. It has been tacitly assumed that ROS production during IR is a non-specific consequence of oxygen interacting with dysfunctional mitochondria upon reperfusion. Recently, this view has changed, suggesting that ROS production during IR occurs by a defined mechanism. Here we survey the metabolic factors underlying IR injury and propose a unifying mechanism for its causes that makes sense of the huge amount of disparate data in this area and provides testable hypotheses and new directions for therapies.
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