斯达
STAT蛋白
贾纳斯激酶
JAK-STAT信号通路
SOCS3
细胞因子信号抑制因子1
细胞因子
细胞因子信号抑制因子
信号转导
癌症研究
炎症
医学
心力衰竭
白细胞介素6
车站3
免疫学
细胞生物学
生物
内科学
抑制器
酪氨酸激酶
癌症
作者
Andrew M. Terrell,Paul R. Crisostomo,George M. Wairiuko,Meijing Wang,Eric D. Morrell,Daniel R. Meldrum
出处
期刊:Shock
[Ovid Technologies (Wolters Kluwer)]
日期:2006-09-01
卷期号:26 (3): 226-234
被引量:100
标识
DOI:10.1097/01.shk.0000226341.32786.b9
摘要
Cytokines are important mediators of cardiac disease. Accumulating evidence indicates that members of the interleukin-6 family of cytokines promote cardiac hypertrophy through the activation of the Janus kinase-signal transducer and activator of transcription (Jak/STAT) pathway. Aberrant Jak/STAT signaling may promote progression from hypertrophy to heart failure. Suppressor of cytokine signaling (SOCS) proteins are underexplored, negative regulators of Jak/STAT signaling. SOCS proteins may also interact with other inflammatory pathways known to affect cardiac function. A better understanding of the therapeutic potential of these proteins may lead to the controlled progression of heart failure and the limitation of myocardial depression. This review summarizes the cardiophysiological effect of the IL-6 cytokine family, outlines the mechanistic pathway of Jak/STAT signaling, explores the regulatory role of SOCS proteins in the heart, and discusses the potential of using SOCS proteins clinically.
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