Mechanisms and Consequences of Inflammatory Signaling in the Myocardium

被引:65
作者
Ahn, Jihyun [1 ]
Kim, Jaetaek [1 ]
机构
[1] Chung Ang Univ, Dept Internal Med, Coll Med, Seoul 156755, South Korea
基金
新加坡国家研究基金会;
关键词
Myocardial inflammation; Ventricular remodeling; Heart failure; Ischemia-reperfusion; Nuclear factor-kappaB; Reactive oxygen species; Cytokine; Chemokine; Inflammasome; Receptor activator of nuclear factor kappaB ligand; Tumor necrosis factor; Interleukin; Protease; Protease-activated receptors; CHRONIC HEART-FAILURE; FACTOR-KAPPA-B; RECEPTOR-STIMULATED APOPTOSIS; PATTERN-RECOGNITION RECEPTORS; PROTEASE-ACTIVATED RECEPTORS; NECROSIS-FACTOR-ALPHA; N-TERMINAL KINASE; VENTRICULAR MYOCYTES; CARDIAC MYOCYTES; IN-VITRO;
D O I
10.1007/s11906-012-0309-0
中图分类号
R6 [外科学];
学科分类号
1002 ; 100210 ;
摘要
To further understand chronic heart disease, such as heart failure and cardiomyopathy, we must fully define signaling pathways within the myocardium. Recent studies suggest that some forms of heart disease are associated with a chronic low-grade inflammation that promotes adverse ventricular remodeling and correlates with disease progression. Several inflammatory mediators, including TNF-alpha, IL-1 beta, and IL-6, are involved in cardiac injury subsequent to myocardial ischemia and reperfusion, sepsis, viral myocarditis, and transplant rejection. Once activated, components of the inflammatory response can have both beneficial and deleterious effects on the heart. In this review, we discuss the complex inflammatory signaling pathways in the myocardium and potential therapeutic implications.
引用
收藏
页码:510 / 516
页数:7
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