醛固酮
新加坡元1
CTGF公司
内科学
内分泌学
螺内酯
上皮钠通道
盐皮质激素受体
盐皮质激素
纤维化
心力衰竭
医学
生物
化学
生长因子
受体
糖皮质激素
钠
有机化学
作者
Beatriz Martín-Fernández,María Valero Muñoz,Natalia de las Heras,Sandra Ballesteros,Vicente Lahera
出处
期刊:Hormone Molecular Biology and Clinical Investigation
[De Gruyter]
日期:2014-02-07
卷期号:18 (2): 53-61
被引量:6
标识
DOI:10.1515/hmbci-2013-0052
摘要
Aldosterone regulates sodium (Na+) and potassium (K+) transports in epithelial cells. Besides, aldosterone participates in cardiac alterations associated with hypertension, heart failure, diabetes, and other pathological alterations. One of the main cardiac alterations induced by aldosterone is cardiac hypertrophy in which different mechanisms are involved such as increased cardiomyocyte, calcium concentration, oxidative stress, and inflammatory and fibrotic mediators stimulation. Many epidemiological studies have demonstrated that left ventricular hypertrophy is associated with significantly increased risk of heart failure and malignant arrhythmias. SGK1 is a member of the serine/threonine kinase gene family that plays an important role in the absorption of Na+ and water through the Na+ channel in the apical membrane of tubular epithelial cells. SGK1 has been related to fibrotic mediator increase such as connective tissue growth factor (CTGF) and transforming growth factor-β (TGF-β) as well as inflammatory [tumor necrosis factor-α (TNF-α) and interleukin (IL)-1β] and oxidative (NADPH oxidase) species. It has been shown that aldosterone induces SGK1 gene expression not only in kidneys but also in the heart. Supporting the central role of SGK1 in cardiac alterations induced by aldosterone, treatment with the mineralocorticoid antagonist spironolactone is able to reduce the gene expression of SGK1 in aldosterone-treated rats. Taken together, data suggest the involvement of SGK1 in a complex intracellular signaling, involving fibrotic, inflammatory, and oxidative pathways, which lead to cardiac hypertrophy and fibrosis induced by aldosterone.
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