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血管矿皮质激素受体激活与疾病。

Vascular mineralocorticoid receptor activation and disease.

机构信息

Laboratorio de Fisiología Cardiovascular y Trasplante Renal, Unidad de Medicina Traslacional, Instituto de Investigaciones Biomédicas, Universidad Nacional Autónoma de México and Instituto Nacional de Cardiología Ignacio Chávez, Mexico City, Mexico.

INSERM U1116, Clinical Investigation Centre, Lorraine University, Vandoeuvre-lès-Nancy, France; INI-CRCT (Cardiovascular and Renal Clinical Trialists) F-CRIN Network, Nancy, France; Centre de Recherche des Cordeliers, INSERM, Sorbonne Université, USPC, Université Paris Descartes, Université Paris Diderot, F-75006, Paris, France.

出版信息

Exp Eye Res. 2019 Nov;188:107796. doi: 10.1016/j.exer.2019.107796. Epub 2019 Sep 12.

DOI:10.1016/j.exer.2019.107796
PMID:31521629
Abstract

Mineralocorticoid receptor activation in endothelial and smooth muscle cells can promote vascular disease by increasing oxidative stress, promoting inflammation, accelerating vascular stiffness, remodeling, and calcification, altering vessel responsiveness to various vasoactive factors, thus altering vascular tone and blood pressure, and by altering angiogenesis. Here, we review the recent evidence highlighting the impact of vascular mineralocorticoid receptor activation in pathological situations, including kidney injury, vascular injury associated with metabolic diseases, atherosclerosis, cerebral vascular injury during hypertension, vascular stiffening and aging, pulmonary hypertension, vascular calcification, cardiac remodeling, wound healing, inflammation, thrombosis, and disorders related to angiogenic defects in the eye. The possible mechanisms implicating mineralocorticoid receptor activation in various vascular disorders are discussed. Altogether, recent evidence points towards pharmacological mineralocorticoid receptor inhibition as a strategy to treat diseases in which overactivation of the mineralocorticoid receptor in endothelial and/or smooth muscle cells may play a pivotal role.

摘要

内皮细胞和血管平滑肌细胞中醛固酮受体的激活可通过增加氧化应激、促进炎症、加速血管僵硬、重塑和钙化、改变血管对各种血管活性因子的反应性,从而改变血管张力和血压,以及改变血管生成,从而促进血管疾病。在这里,我们回顾了最近的证据,强调了血管醛固酮受体激活在病理情况下的影响,包括肾损伤、与代谢疾病相关的血管损伤、动脉粥样硬化、高血压期间的脑血管损伤、血管僵硬和衰老、肺动脉高压、血管钙化、心脏重塑、伤口愈合、炎症、血栓形成以及与眼部血管生成缺陷相关的疾病。讨论了涉及各种血管疾病的醛固酮受体激活的可能机制。总之,最近的证据表明,药理抑制醛固酮受体可能是治疗醛固酮受体在内皮细胞和/或血管平滑肌细胞过度激活可能起关键作用的疾病的一种策略。

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