Shigetaka Yoshida

TL;DR: Evidence is provided that signaling cross-talk between Rac1 and mineralocorticoid receptor modulates mineralocortex receptor activity and Rac1 is identified as a therapeutic target for chronic kidney disease.

TL;DR: In this article, the effects of aldosterone on podocyte, a key player of the glomerular filtration barrier, were investigated in uninephrectomized rats and fed a high-salt diet, where the podocyte injury was accompanied by renal reduced nicotinamide-adenine dinucleotide phosphate oxidase activation, increased oxidative stress, and enhanced expression of Sgk1.

TL;DR: It is suggested that podocyte injury underlies the glomerulopathy of Dahl salt-hypertensive rats and that inhibition of aldosterone by eplerenone is protective against podocyte damage, proteinuria, and glomerumulosclerosis in this hypertensive model.

TL;DR: The data suggest that adipocyte-derived factors other than angiotensin II might contribute to the aldosterone excess of this model, and SHR/NDmcr-cp exhibit enhanced ald testosterone signaling, podocyte injury, and proteinuria, which are ameliorated by eplerenone or tempol.

TL;DR: It is shown that high-salt loading activates Rac1 in the kidneys in rodent models of salt-sensitive hypertension, leading to blood pressure elevation and renal injury via an MR-dependent pathway and is confirmed as a determinant of salt sensitivity in mice lacking Rho GDP-dissociation inhibitor α.