Oxidative stress in heart failure or during ischemia/reperfusion occurs as a result of the excessive generation or accumulation of free radicals or their oxidation products. Free radicals formed during oxidative stress can initiate lipid peroxidation, oxidize proteins to inactive states and cause DNA strand breaks. Oxidative stress is a condition in which oxidant metabolites exert toxic effects because of their increased production or an altered cellular mechanism of protec- tion. In the early phase of acute heart ischemia cytokines have the feature to be functional pleiotropy and redundancy, moreover, several cytokines exert similar and overlapping actions on the same cell type and one cytokine shows a wide range of biological effects on various cell types. Activation of cytokine cascades in the infarcted myocardium was estab- lished in numerous studies. In experimental models of myocardial infarction, induction and release of the pro- inflammatory cytokines like TNF- (Tumor Necrosis Factor ), IL-1 (Interleukin-1) and IL-6 (Interleukin-6) and chemokines are steadily described. The current review examines the role of oxidative stress and pro-inflammatory cytoki- nes response following acute myocardial infarction and explores the inflammatory mechanisms of cardiac injury.
Cardiac Oxidative Stress and Inflammatory Cytokines Response After Myocardial Infarction.
NERI, MARGHERITA;POMARA, CRISTOFORO;RIEZZO, IRENE;TURILLAZZI, EMANUELA;
2013-01-01
Abstract
Oxidative stress in heart failure or during ischemia/reperfusion occurs as a result of the excessive generation or accumulation of free radicals or their oxidation products. Free radicals formed during oxidative stress can initiate lipid peroxidation, oxidize proteins to inactive states and cause DNA strand breaks. Oxidative stress is a condition in which oxidant metabolites exert toxic effects because of their increased production or an altered cellular mechanism of protec- tion. In the early phase of acute heart ischemia cytokines have the feature to be functional pleiotropy and redundancy, moreover, several cytokines exert similar and overlapping actions on the same cell type and one cytokine shows a wide range of biological effects on various cell types. Activation of cytokine cascades in the infarcted myocardium was estab- lished in numerous studies. In experimental models of myocardial infarction, induction and release of the pro- inflammatory cytokines like TNF- (Tumor Necrosis Factor ), IL-1 (Interleukin-1) and IL-6 (Interleukin-6) and chemokines are steadily described. The current review examines the role of oxidative stress and pro-inflammatory cytoki- nes response following acute myocardial infarction and explores the inflammatory mechanisms of cardiac injury.I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.
