Cardiac hypertrophy and fibrosis in the metabolic syndrome: a role for aldosterone and the mineralocorticoid receptor.
Cardiac hypertrophy and fibrosis in the metabolic syndrome: a role for aldosterone and the mineralocorticoid receptor.
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DOI：
10.4061/2011/346985
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发表时间：
2011
影响因子：
1.9
通讯作者：
Sam F
中科院分区：
文献类型：
--
作者：
Essick EE;Sam F
肥胖和高血压是代谢综合征的主要危险因素，使个体易患心血管并发症的风险增加，如不良心脏重塑和心力衰竭。已经有很多研究表明，在代谢综合征的发病机制中，肾素-血管紧张素-醛固酮系统（RAAS）的增加起作用，特别是醛固酮如何介导左心室肥大和增加心脏纤维化通过其与盐皮质激素受体（MR）的相互作用。在此，我们回顾了肥胖与醛固酮升高以及与代谢综合征相关的心脏肥大和纤维化的相关发现。这些研究说明了脂肪组织、心脏和肾上腺皮质之间复杂的相互作用。此外，我们还讨论了我们实验室的发现，这些发现表明代谢综合征中的心脏肥大和纤维化可能涉及醛固酮和脂肪因子（如脂联素）之间的相互作用。
Obesity and hypertension, major risk factors for the metabolic syndrome, render individuals susceptible to an increased risk of cardiovascular complications, such as adverse cardiac remodeling and heart failure. There has been much investigation into the role that an increase in the renin-angiotensin-aldosterone system (RAAS) plays in the pathogenesis of metabolic syndrome and in particular, how aldosterone mediates left ventricular hypertrophy and increased cardiac fibrosis via its interaction with the mineralocorticoid receptor (MR). Here, we review the pertinent findings that link obesity with elevated aldosterone and the development of cardiac hypertrophy and fibrosis associated with the metabolic syndrome. These studies illustrate a complex cross-talk between adipose tissue, the heart, and the adrenal cortex. Furthermore, we discuss findings from our laboratory that suggest that cardiac hypertrophy and fibrosis in the metabolic syndrome may involve cross-talk between aldosterone and adipokines (such as adiponectin).