盐皮质激素受体
内分泌学
蛋白尿
内科学
盐皮质激素
上皮钠通道
肾
醛固酮
肾脏疾病
远曲小管
生物
医学
重吸收
化学
钠
有机化学
作者
Amin Abedini,Andrea Sánchez‐Navarro,Junnan Wu,Konstantin A. Klötzer,Ziyuan Ma,Bibek Poudel,Tomohito Doke,Michael S. Balzer,Julia Frederick,Hana Černecká,Hongbo Liu,Xiujie Liang,Steven Vitale,Peter Kolkhof,Katalin Suszták
摘要
Mineralocorticoid excess commonly leads to hypertension and kidney disease. In our study, we employed single-cell expression and chromatin accessibility tools to characterize the mineralocorticoid target genes and cell types. We demonstrated that mineralocorticoid effects are established through open chromatin and target gene expression, primarily in principal and connecting tubule cells, and to a lesser extent, in segments of the distal convoluted tubule cells. We examined the kidney-protective effects of steroidal and non-steroidal mineralocorticoid antagonists (MRAs), as well as amiloride, an epithelial sodium channel inhibitor, in a rat model of deoxycorticosterone acetate, unilateral nephrectomy, and high salt consumption-induced hypertension and cardiorenal damage. All antihypertensive therapies protected from cardiorenal damage. However, finerenone was particularly effective in reducing albuminuria and improving gene expression changes in podocytes and proximal tubule cells, even with equivalent blood pressure reduction.
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