Pathological mechanisms of chemokines involved in reperfusion injury following myocardial ischemia

Abstract

Myocardial ischemia is the most frequent form of cardiovascular disease with high morbidity and mortality, for which timely restoration of blood flow to the ischemic myocardium (reperfusion) is indispensable for a better patient outcome. After ischemic/reperfusion injury, increased vascularization or increased vascular protection may be critical to mediate functional recovery, with endothelial cells being the primary effector cell type responsible for neo-vascularization and angiogenesis. Chemokines are small proinflammatory proteins that act as both chemoattractant and activators of leukocytes. Chemokines are considered as a subset of the cytokine family responsible for cell migration, activation, and tissue injury. This reviews analysis the pathological mechanisms of myocardial ischemia/reperfusion (I/R) and identify circulating inflammatory chemokines of significance involved in reperfusion injury and the interventions for different pathways and targets, with evidence that chemokines antibody could reduce cardiac inflammation and protect the heart from I/R injury via inhibition of the activity of NF-κB, ICAM-1 expression, and MPO activities in different I/R model.