Key result
Proinflammatory cytokines drive myocardial dysfunction and cardiomyocyte necrosis in ischemia-reperfusion injury.
Why the study?
Cytokines such as TNF-alpha, IL-1, and IL-6 contribute to ischemia-reperfusion injury, but their mechanisms and roles remain controversial and need better definition.
Answers are grounded in this paper and cite their sources.
Cytokine role in I/R injury supports targeted trials; leaves open practice change pending randomized data.
Extensive investigations have implicated cytokines such as tumour necrosis factor (TNF)- alpha and interleukin (IL)-1, and IL-6 as contributing to the pathology of ischemia-reperfusion (I/R) injury, since an increase in the production of those cytokines was clinically detected after myocardial infarction and cardiopulmonary bypass surgery. Current evidence indicates that these cytokines are autocrine contributors to myocardial dysfunction and cardiomyocyte necrosis in I/R injury, whereas, earlier evidence also suggest that cytokines have controversial roles in cardiovascular pathophysiology. Accordingly, it becomes vital to better define the mechanisms of action of cytokines as important steps towards the development of effective therapeutic strategies to combat their deleterious effects in ischemia-induced myocardial injury. Since TNF-alpha, TGF-beta1, IL-1, IL-6 and IL-8 have been frequently studied in cardiovascular diseases, especially in I/R heart disease, the purpose of this article is to review the cardiodepressant role of these cytokines and their release in I/R injury.
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Zhang et al. (2008) conducted a review in Ischemia-reperfusion (I/R) heart injury. Cytokines (TNF-alpha, TGF-beta1, IL-1, IL-6, IL-8) was evaluated. Cytokines such as TNF-alpha, TGF-beta1, IL-1, IL-6, and IL-8 act as autocrine contributors to myocardial dysfunction and cardiomyocyte necrosis in ischemia-reperfusion injury.
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