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代谢综合征中的盐皮质激素受体。

Mineralocorticoid receptors in the metabolic syndrome.

机构信息

INSERM, U970, Paris Cardiovascular Research Center - PARCC, 75015 Paris, France.

出版信息

Trends Endocrinol Metab. 2009 Nov;20(9):444-51. doi: 10.1016/j.tem.2009.05.006. Epub 2009 Sep 30.

Abstract

The mineralocorticoid receptor (MR) mediates aldosterone effects on salt homeostasis and blood pressure regulation. MR activation also promotes inflammation, cardiovascular remodelling and endothelial dysfunction, and affects adipose tissue differentiation and function. Some of these effects derive from MR activation by glucocorticoids. Recent epidemiological studies show that the incidence of metabolic syndrome increases across quartiles of aldosterone, implicating the MR as a central player in metabolic homeostasis, involving electrolyte, water and energy balance. This review summarizes the current understanding of MR-mediated effects in diverse tissues and the role of aldosterone as a cardiometabolic risk factor, and discusses the possible relationship between inappropriate MR activation (by both mineralocorticoids and glucocorticoids) and the development of metabolic syndrome.

摘要

盐皮质激素受体(MR)介导醛固酮对盐稳态和血压调节的作用。MR 的激活还促进炎症、心血管重塑和内皮功能障碍,并影响脂肪组织分化和功能。这些作用中的一些源自糖皮质激素对 MR 的激活。最近的流行病学研究表明,随着醛固酮四分位数的增加,代谢综合征的发病率增加,提示 MR 是代谢稳态的核心参与者,涉及电解质、水和能量平衡。本文综述了目前对 MR 在不同组织中的介导作用以及醛固酮作为心脏代谢风险因素的认识,并讨论了不合适的 MR 激活(由盐皮质激素和糖皮质激素引起)与代谢综合征发展之间的可能关系。

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