期刊
ACTA PHYSIOLOGICA
卷 228, 期 2, 页码 -出版社
WILEY
DOI: 10.1111/apha.13390
关键词
endothelium; Macrophages; renal fibrosis; T cells; vascular smooth muscle
类别
资金
- Institut National de la Sante et de la Recherche Medicale
- Centre de Recherche Industrielle et Technique
- Agence Nationale de la Recherche [ANR-16-CE14-0021-01]
- Fight-HF Avenir investment program [ANR-15-RHUS-0004]
- French Medical Research Foundation [DEQ20160334885]
- FP7 [BM1301]
- National Autonomous University of Mexico-DGAPA-PAPIIT [IN202919]
Mineralocorticoid receptor (MR) activation in the kidney can occur outside the aldosterone-sensitive distal nephron in sites including the endothelium, smooth muscle and inflammatory cells. MR activation in these cells has deleterious effects on kidney structure and function by promoting oxidative injury, endothelial dysfunction and stiffness, vascular remodelling and calcification, decreased relaxation and activation of T cells and pro-inflammatory macrophages. Here, we review the data showing the cellular consequences of MR activation in endothelial, smooth muscle and inflammatory cells and how this affects the kidney in pathological situations. The evidence demonstrating a benefit of pharmacological or genetic MR inhibition in various models of kidney disease is also discussed.
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