Journal
CURRENT HYPERTENSION REPORTS
Volume 14, Issue 6, Pages 510-516Publisher
SPRINGER
DOI: 10.1007/s11906-012-0309-0
Keywords
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
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Funding
- National Research Foundation of Korea (NRF)
- Ministry of Education, Science and Technology [2012R1A1A2008177, 2012-0003804]
- National Research Foundation of Korea [2012R1A1A2008177] Funding Source: Korea Institute of Science & Technology Information (KISTI), National Science & Technology Information Service (NTIS)
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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.
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