Cellular cross-talk between epicardial adipose tissue and myocardium in relation to the pathogenesis of cardiovascular disease

被引:166
作者
Cherian, Sam [1 ]
Lopaschuk, Gary D. [2 ]
Carvalho, Eugenia [1 ,3 ]
机构
[1] Univ Coimbra, Ctr Neurosci & Cell Biol, P-3004517 Coimbra, Portugal
[2] Univ Alberta, Mazankowski Alberta Heart Inst, Dept Pediat, Edmonton, AB, Canada
[3] Portuguese Diabet Assoc, Lisbon, Portugal
来源
AMERICAN JOURNAL OF PHYSIOLOGY-ENDOCRINOLOGY AND METABOLISM | 2012年 / 303卷 / 08期
关键词
heart adiposity; cardiomyocyte; fatty acid oxidation; lipotoxicity; adipocytokines; adipose tissue; NECROSIS-FACTOR-ALPHA; FACTOR-KAPPA-B; VISCERAL ABDOMINAL FAT; N-TERMINAL KINASE; INSULIN-RESISTANCE; PERICARDIAL FAT; METABOLIC SYNDROME; RISK-FACTORS; CORONARY ATHEROSCLEROSIS; DIASTOLIC DYSFUNCTION;
D O I
10.1152/ajpendo.00061.2012
中图分类号
R5 [内科学];
学科分类号
100201 [内科学];
摘要
Cherian S, Lopaschuk GD, Carvalho E. Cellular cross-talk between epicardial adipose tissue and myocardium in relation to the pathogenesis of cardiovascular disease. Am J Physiol Endocrinol Metab 303: E937-E949, 2012. First published August 14, 2012; doi: 10.1152/ajpendo.00061.2012.-Epicardial and perivascular fat depot size is considered an index of cardiac and visceral obesity. The functional and anatomic proximity of epicardial adipose tissue (EAT) to myocardium has drawn increasing attention in recent years among researchers attempting to elucidate its putative role as an endocrine organ. This includes the role of EAT as a lipid storing depot and as an inflammatory tissue secreting cytokines and chemokines under pathogenic conditions such as cardiovascular diseases. In this review, we discuss the current state of knowledge regarding the potential EAT mediators of inflammation and the paracrine cross-talk between EAT and the underlying myocardium. We also highlight the most recent findings on the causes and correlates of myocardial steatosis/cardiac lipotoxicity and its association with cardiac dysfunction.
引用
收藏
页码:E937 / E949
页数:13
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