Cardiac Ischemia and Reperfusion

Cardiac ischemia occurs when blood flow to the heart muscle is interrupted, and while restoring that flow is essential for survival, the act of reperfusion itself triggers a second wave of cellular damage driven by reactive oxygen species, calcium overload, and the sudden opening of the mitochondrial permeability transition pore. Understanding this paradox — that the cure carries its own injury — has become central to reducing the death and dysfunction that follow myocardial infarction, which remains one of the leading causes of mortality worldwide. Researchers have found that brief, controlled cycles of ischemia applied either to the heart or to distant tissue before or during a major cardiac event can substantially limit reperfusion damage, a phenomenon known as ischemic and remote ischemic conditioning, though translating these protective effects reliably into clinical outcomes has proven difficult. Active work focuses on mapping the precise signaling cascades that distinguish lethal from survivable cell stress, and on identifying whether interventions targeting mitochondrial function or oxidative pathways can be timed and dosed effectively in real patients.

Works

61,592

Total citations

1,199,644

Keywords

Ischemia-Reperfusion InjuryCardioprotectionMitochondrial Permeability Transition PoreOxidative StressIschemic PreconditioningRemote Ischemic Conditioning