Molecular Mechanisms and Treatment of Ischemia–Reperfusion Injury

Dear Colleagues,

Ischemia–reperfusion (I/R) injury is caused by a temporary restriction of blood supply to a particular organ, such as the heart, brain, kidney, liver and skeletal muscle. Subsequent reperfusion to these hypoxic or anoxic organs causes organ dysfunction and tissue cell death, sometimes leading to systemic circulatory shock. Although the organ type, as well as magnitude and duration of the interruption in the blood supply are critical determinants of whether the organ becomes necrotic or not, organ damage is essentially caused by oxidative stress following reperfusion, which induces cell membrane lipid peroxidation, mitochondrial dysfunction and subsequent inflammatory responses, such as neutrophil activation and the release of reactive oxygen species and other inflammatory mediators, including adhesion molecules and various cytokines. Effective pharmacological agents and methods to combat I/R injury have recently been developed. Nevertheless, we are far from establishing the treatment for this disease. I, therefore, look forward to fruitful discussions on this theme, particularly from the standpoint of molecular biology, and call for original articles and reviews focusing on the pathophysiology of I/R injury, development of animal models, and development of new pharmacological and interventional strategies. This Special Issue will provide a key resource to the readers of CIMB, including new findings related to I/R injury with the potential to lead to novel treatment strategies. 

Prof. Dr. Jun Kobayashi
Guest Editor

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• ischemia–reperfusion injury
• myocardial infarction
• cerebral infarction
• renal infarction
• crush syndrome
• oxidative stress
• reactive oxygen species