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Current Vascular Pharmacology


ISSN (Print): 1570-1611
ISSN (Online): 1875-6212

Cardiac Oxidative Stress and Inflammatory Cytokines Response after Myocardial Infarction

Author(s): Margherita Neri*, Vittorio Fineschi, Marco Di Paolo, Cristoforo Pomara, Irene Riezzo, Emanuela Turillazzi and Daniela Cerretani

Volume 13, Issue 1, 2015

Page: [26 - 36] Pages: 11

DOI: 10.2174/15701611113119990003

Price: $65


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 protection. 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 established in numerous studies. In experimental models of myocardial infarction, induction and release of the pro-inflammatory cytokines like TNF-α (Tumor Necrosis Factor α), IL-1β (Interleukin- 1β) and IL-6 (Interleukin-6) and chemokines are steadily described. The current review examines the role of oxidative stress and pro-inflammatory cytokines response following acute myocardial infarction and explores the inflammatory mechanisms of cardiac injury.

Keywords: Cardiac oxidative stress, Chemokine, IL-1β, IL-6, MCP-1, Myocardial infarction, TNF-α

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