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The role of peroxiredoxins in ischemia-reperfusion-induced cardiac damage

机译:过氧化物氧还蛋白在缺血再灌注引起的心脏损伤中的作用

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摘要

myocardial ischemia related to infarction is a disease of multiple pathways with variable outcomes. Both ischemia and reperfusion contribute to cell and tissue damage after cardiac infarction. Myocardial ischemia-reperfusion initiates maldistribution of ions and various signaling mechanisms, leading to oxidative injury and inflammatory responses that include liberation of cytokines (16) and free radicals (14), up- and downregulation of various genes and their proteins (1,5, 20), and cell death by apoptosis (13) and/or necrosis (11). The treatment of myocardial infarction is currently mostly directed at restoration of blood flow to the previously ischemic area and reduction of oxygen demand of the heart. However, during reperfusion of cardiac tissue, depending on the duration of the previous ischemic event, the heart undergoes additional damage due to the activation of various pathways, functional and physiological impairments, leading to cell death
机译:与梗死有关的心肌缺血是一种多途径,预后不一的疾病。心肌梗塞后,缺血和再灌注均导致细胞和组织损伤。心肌缺血再灌注会引发离子的分布不均和各种信号传导机制,导致氧化损伤和炎症反应,包括细胞因子(16)和自由基(14)的释放,各种基因及其蛋白质的上调和下调(1,5, 20),以及由于凋亡(13)和/或坏死(11)造成的细胞死亡。心肌梗塞的治疗目前主要针对恢复到先前缺血区域的血流和减少心脏的氧需求。但是,在心脏组织的再灌注过程中,根据先前缺血事件的持续时间,由于各种途径的激活,功能和生理损伤,心脏会遭受额外的损害,从而导致细胞死亡

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