Journal
CELL METABOLISM
Volume 23, Issue 2, Pages 254-263Publisher
CELL PRESS
DOI: 10.1016/j.cmet.2015.12.009
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Funding
- 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
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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.
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