[Figure: see text].
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| http://dx.doi.org/10.1161/HYPERTENSIONAHA.121.17263 | DOI Listing |
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Relations between glomerular hyperfiltration and podocyte injury: potential role of Piezo1 in the Rac1-mineralocorticoid receptor activation pathway.
Hypertens Res
April 2024
Department of Endocrinology, Metabolism, Rheumatology and Nephrology, Faculty of Medicine, Oita University, Yufu, Japan.
Activation of Rac1-Mineralocorticoid Receptor Pathway Contributes to Renal Injury in Salt-Loaded Mice.
Hypertension
July 2021
Division of Clinical Epigenetics, Research Center for Advanced Science and Technology, The University of Tokyo, Japan (D.H., M.N., N.A., W.K., S.O., S.S., T.M., T.F.).
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View Article and Find Full Text PDFMechanism of salt-sensitive hypertension: focus on adrenal and sympathetic nervous systems.
J Am Soc Nephrol
June 2014
Department of Clinical Epigenetics, Research Center for Advanced Science and Technology, The University of Tokyo, Tokyo, Japan; and CREST, Tokyo, Japan
A central role for the kidney among the systems contributing to BP regulation and the development of hypertension has been proposed. Both the aldosterone/mineralocorticoid receptor pathway and the renal sympathetic nervous system have important roles in the regulation of renal excretory function and BP control, but the mechanisms underlying these processes have remained unclear. However, recent studies revealed the activation of two pathways in salt-sensitive hypertension.
View Article and Find Full Text PDFAberrant Rac1-mineralocorticoid receptor pathways in salt-sensitive hypertension.
Clin Exp Pharmacol Physiol
December 2013
Division of Clinical Epigenetics, Research Center for Advanced Science and Technology=1, The University of Tokyo=1, Tokyo, Japan.
According to Guyton's model, impaired renal sodium excretion plays a key role in the increased salt sensitivity of blood pressure (BP). Several factors contribute to impaired renal sodium excretion, including the sympathetic nervous system, the renin-angiotensin system and aldosterone. Accumulating evidence suggests that abnormalities in aldosterone and its receptor (i.
View Article and Find Full Text PDFRole of Rac1-mineralocorticoid-receptor signalling in renal and cardiac disease.
Nat Rev Nephrol
February 2013
Division of Chronic Kidney Disease, Department of Nephrology and Endocrinology, The University of Tokyo Graduate School of Medicine, 7-3-1 Hongo, Bunkyo-ku, Tokyo 113-8655, Japan.
The Rho-family small GTPase, Ras-related C3 botulinum toxin substrate 1 (Rac1), has been implicated in renal and cardiac disease. Rac1 activation in podocytes has been shown in several models of proteinuric kidney disease and a concept involving motile podocytes has been proposed. Evidence also exists for a critical role of Rac1-mediated oxidative stress in cardiac hypertrophy, cardiomyopathy and arrhythmia, and of the aldosterone-mineralocorticoid-receptor system in proteinuria and cardiac disorders.
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