炎症细胞因子tnf-α在心衰发生机制中的作用（The role of inflammatory cytokine tnf- alpha in the pathogenesis of heart failure）.docVIP

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炎症细胞因子tnf-α在心衰发生机制中的作用（The role of inflammatory cytokine tnf- alpha in the pathogenesis of heart failure）.doc

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炎症细胞因子tnf-α在心衰发生机制中的作用（The role of inflammatory cytokine tnf- alpha in the pathogenesis of heart failure）

炎症细胞因子tnf-α在心衰发生机制中的作用（The role of inflammatory cytokine tnf- alpha in the pathogenesis of heart failure） The role of inflammatory cytokine TNF- alpha in the pathogenesis of heart failure Clinical class four Wang Yaosun, Yao Yao, Yao Ru Zhou, Qin Ying, Qin Ying, Li Jianing Over expression of inflammatory cytokines in heart failure often in patients affected by myocardial contractility, causes cardiac hypertrophy, myocardial fibrosis and apoptosis induction, promote cardiac remodeling, promote the occurrence and development of heart failure, and inflammation factors indicates that adverse cardiovascular events, will be the new target of anti-inflammatory treatment of heart failure. This article will explain the role of inflammatory cytokines in heart failure. 1 the relationship between inflammatory cytokines and heart failure Inflammatory cytokines are endogenous polypeptides produced mainly by immune cells and have many powerful biological effects. They can mediate a variety of immune responses. Heart failure in patients with inflammatory markers such as C-reactive protein C (CRP), tumor necrosis factor alpha (TNF- alpha), interleukin 1 (IL-1), interleukin 6 (interleukin-6, IL-6), monocyte chemoattractant protein -1 (MCP-1) is proportional to the severity of heart failure and increased level. Cytokines, such as serum TNF - alpha, were independent risk factors for predicting survival. 2 inflammatory cytokine production during heart failure Proinflammatory cytokines such as TNF-, IL-1, and IL-6 are not expressed in the normal heart, and these cytokines are up-regulated, synthesized and released when the myocardium is damaged. In the course of heart failure, cytokines are produced mainly through 3 pathways: (1) stress pathway: ischemia, hypoxia, infection can activate mitogen activated protein kinase (MAPK), signal transducer and activator of transcription (STAT) and calcineurin (calcineurin) pathway, these signaling pathways and activating transcription factor kappa B