Cardiac Oxidative Stress and Inflammatory Cytokines Response after Myocardial Infarction
Cardiac Oxidative Stress and Inflammatory Cytokines Response after Myocardial Infarction
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DOI：
10.2174/15701611113119990003
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发表时间：
2015-01-01
影响因子：
4.5
通讯作者：
Cerretani, Daniela
中科院分区：
文献类型：
--
作者：
Neri, Margherita;Fineschi, Vittorio;Cerretani, Daniela
心力衰竭或缺血/再灌注期间的氧化应激是由于自由基或其氧化产物的过度产生或积累而发生的。在氧化应激过程中形成的自由基可以引发脂质过氧化，将蛋白质氧化成非活性状态并导致DNA链断裂。氧化应激是一种氧化代谢物由于其产量增加或细胞保护机制改变而产生毒性作用的状况。在急性心肌缺血早期，细胞因子具有功能多效性和冗余性的特点，而且几种细胞因子对同一细胞类型具有相似和重叠的作用，一种细胞因子对多种细胞类型具有广泛的生物学效应。在许多研究中确立了梗死心肌中细胞因子级联的激活。在心肌梗塞的实验模型中，促炎细胞因子如TNF-α（肿瘤坏死因子α）、IL-1 β（白细胞介素-1 β）和IL-6（白细胞介素-6）和趋化因子的诱导和释放被稳定地描述。本文综述了急性心肌梗死后氧化应激和促炎细胞因子反应的作用，并探讨了心肌损伤的炎症机制。
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-alpha (Tumor Necrosis Factor alpha), IL-1 beta (Interleukin-1 beta) 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.