Pathophysiology of Ischemia-Reperfusion Injury: Molecular Mechanisms and Organ-Specific Effects

Ischemia-reperfusion (I/R) injury is a pathological process that occurs when blood supply returns to tissue after a period of ischemia. While reperfusion is necessary to prevent permanent tissue damage, it paradoxically exacerbates cellular injury through oxidative stress, inflammation, and apoptosis. This review summarizes the molecular mechanisms underlying I/R injury, emphasizing organ-specific responses in the heart, brain, kidney, and liver. Understanding these pathways provides insights into therapeutic strategies to mitigate damage and improve clinical outcomes. Ischemia-reperfusion (I/R) injury represents a paradoxical exacerbation of tissue damage occurring upon restoration of blood flow following a period of restricted perfusion. This phenomenon involves a complex interplay of oxidative stress, inflammatory cascades, calcium dysregulation, mitochondrial destabilization, and programmed cell death pathways. Distinct cellular populations and metabolic characteristics in organs such as the myocardium, cerebral tissue, kidneys, and liver confer variable susceptibility and injury patterns. The present review synthesizes current molecular insights, highlighting signaling networks including ROS generation, NF-κB activation, mitochondrial permeability transitions, and pro-apoptotic factor release. Understanding these mechanisms is critical for devising precise interventions aimed at minimizing functional impairment and improving post-ischemic recovery outcomes.