The role of proinflammatory cytokines in regulation of cardiac bioelectrical activity: link to mechanoelectrical feedbackстатья

Дата последнего поиска статьи во внешних источниках: 29 мая 2015 г.

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[1] The role of proinflammatory cytokines in regulation of cardiac bioelectrical activity: link to mechanoelectrical feedback / V. Kuzmin, D. Abramochkin, V. Mitrochin et al. // Mechanical stretch and cytokines. — Vol. 5 of Mechanosensitivity in Cells and Tissues. — Springer Science+Business Media B.V Amsterdam, Netherlands, 2012. — P. 107–154. In this review we cover key issues, concerned with the effects of cytokines in cardiac tissue and cardiac cells. We discuss the effects of proinflammatory cytokines under non-pathological conditions and their mechanisms dependent and independent of nitric oxide. The role of proinflammatory cytokines is considered in acute myocardial infarction and in heart failure. We also describe proinflammatory cytokines as inductors of arrhythmia. We discuss ionic current alternation as possible mechanisms of cytokines action in heart. We consider TNF-α as a possible player in this signaling cascade. It was shown that TNF-α induced alternation of transmembrane action potentials. Influence of TNF-α on transient outward current (I to), I Kur, I Kr, I Ks, I K1 is also reported. We discuss the interplay between TNF-α and Ca2+ current, influence of TNF-α on SERCA. Then we consider influence of IL-1 on action potentials, I Na, I Ca, I K. We also address the role of IL-2, IL-6, and IL-11. Finally using TNF-α and IL-6 as an example we discuss the effects of cytokines on mechanoelectrical feedback. Perfusion of cardiac tissue with TNF-α containing solution leads to abnormalities in cardiac electrical activity, majorly to prolongation of APD90 and appearance of hump-like depolarization at APD90 level. After reaching E c hump-like depolarization transforms into extra-AP, leading to sustained arrhythmias. TNF-α activates NO cardiomyocyte synthases and the rise of intracellular NO levels opens MGCs, which leads to sodium entry into the cell, which depolarizes cellular membrane, shifting resting potential towards E C. We proposed and proved that TNF-α triggered arrhythmias can be mediated through activation of MGCs. Stretching of preparations removed TNF-α. Perfusion of preparation with IL-6 containing solution leads to fibrillation in response to low levels of stretch. IL-6 mechanisms of action are mediated by NO synthases in cardiomyocytes. The circulating levels of TNF-α and IL-6 were found to be significantly higher in patients suffering from atrial fibrillation. It suggests a positive feedback between inflammation and atrial fibrillation. Proinflammatory cytokines are believed to be markers of atrial fibrillation, and more over, the key element in this positive feedback system. [ DOI ]

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