作者: Nicholas C. Bene , Pilar Alcaide , Henry H. Wortis , Iris Z. Jaffe
DOI: 10.1016/J.STEROIDS.2014.04.005
关键词: Pathophysiology of hypertension 、 Macrophage 、 Lymphocyte 、 T lymphocyte 、 Immunology 、 Antigen 、 Pathogenesis 、 Mineralocorticoid receptor 、 Immune system 、 Biology
摘要: Mineralocorticoid receptors (MRs) contribute to the pathophysiology of hypertension and cardiovascular disease in humans. As such, MR antagonists improve outcomes but molecular mechanisms remain unclear. The actions kidney increase blood pressure are well known, recent identification MRs immune cells has led novel discoveries pathogenesis that reviewed here. regulates macrophage activation pro-inflammatory M1 phenotype this process contributes fibrosis response mouse models stroke. T lymphocytes have recently been implicated development models. vivo promotes lymphocyte differentiation Th1 Th17 subsets while decreasing number anti-inflammatory regulatory lymphocytes. mechanism likely involves antigen presenting dendritic subsequently regulate Th1/Th17 polarization by production cytokines. Alteration balance between helper atherosclerosis associated complications. B also express specific lymphocyte-derived antibodies modulate progression atherosclerosis. However, role function remains be explored. Overall, studies identified new which may organ damage patients with risk factors. Conversely, inhibition leukocyte protective effects antagonist drugs patients. Further understanding could yield drug targets for disease.