Tumor necrosis factor receptor-associated factor 6 as a nuclear factor kappa B-modulating, therapeutic target in cardiovascular diseases: at the heart of it all

被引:27
作者
Abdullah, Muhammad
Berthiaume, Jessica M.
Willis, Monte S.
机构
[1] Quaid I Azam Univ, Dept Biochem, Islamabad, Pakistan
[2] Univ N Carolina, Dept Pathol & Lab Med, Chapel Hill, NC 27599 USA
[3] Case Western Reserve Univ, Dept Physiol & Biophys, Cleveland, OH 44106 USA
[4] Univ N Carolina, Dept Pharmacol, Chapel Hill, NC 27599 USA
基金
美国国家卫生研究院;
关键词
MYOCARDIAL ISCHEMIA/REPERFUSION INJURY; CARDIAC DYSFUNCTION; INNATE IMMUNITY; EXTRACELLULAR HISTONES; INFLAMMATORY RESPONSES; POLYMICROBIAL SEPSIS; ADAPTIVE IMMUNITY; ISCHEMIC-STROKE; FAILING HEART; TRAF6;
D O I
10.1016/j.trsl.2017.10.012
中图分类号
R446 [实验室诊断]; R-33 [实验医学、医学实验];
学科分类号
1001 ;
摘要
Inflammatory and immune signaling has been documented as a root cause of many cardiovascular pathologies. In this review, we explore the emerging role of tumor necrosis factor receptor-associated factor 6 (TRAF6)-nuclear factor kappa B (NF-kappa B) signaling axis in atherosclerosis, ischemic heart disease, pathologic cardiac hypertrophy or heart failure, myocarditis, and sepsis-induced cardiomyopathy. We discuss the current understanding of cardiac inflammation in heart disease, present the TRAF6 signaling axis in the heart, then summarize what is known about TRAF6 in pathophysiology of heart disease including proof-of-concept studies that identify the utility of blocking TRAF6 to attenuate cardiac dysfunction, which suggests that TRAF6 is a novel, druggable target in treating cardiovascular disease incurred by inflammatory processes.
引用
收藏
页码:48 / 61
页数:14
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