Cessation of blood flow during an ischemic event, such as myocardial or cerebral infarction or cardiac arrest, leads to loss of oxygen and nutrient supply, accumulation of metabolites, and consequently to injured tissue in the affected organ(s). Reperfusion, or the restoration of blood flow as early as possible, is therapeutically indicated. Paradoxically, reperfusion itself can lead to additional tissue damage that might be similarly detrimental or even worse than the initial ischemic injury. During ischemia, anaerobe metabolism and lactate accumulation lead to acidosis and decreased adenosine triphosphate (ATP) levels. Consequently, ATP-dependent ion transporters become dysfunctional, resulting in intracellular calcium overload. Moreover, mitochondria are intimately involved in ischemia/reperfusion injury by generation of reactive oxygen species and the opening of the mitochondrial permeability transition pore. Mitochondrial swelling, rupture, and fragmentation are among the intracellular consequences of ischemia/reperfusion injury.

In this Methods Collection, we plan to include manuscripts describing current and new techniques to assess, attenuate, or prevent ischemia/reperfusion injury in different in vitro, ex vivo, and in vivo models as a resource for interested scientists in this clinically relevant area of research.