ReviewClinical and experimental nephrology2014
Mineralocorticoid receptor activation as an etiological factor in kidney diseases.
Review in Clinical and experimental nephrology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 14 citations in OpenAlex.
- Chinese Expert Consensus on the Clinical Application of Finerenone in Geriatric Comorbidities: Geriatrics Branch of Chinese Medical Association, Cardiovascular Group of Geriatrics Branch of Chinese Medical Association.Aging medicine (Milton (N.S.W)) · 2026Article
- Review of mechanisms and frontier applications in IL-17A-induced hypertension.Open medicine (Warsaw, Poland) · 2025Review
- Effects of the novel nonsteroidal mineralocorticoid receptor blocker, esaxerenone (CS-3150), on blood pressure and urinary angiotensinogen in low-renin Dahl salt-sensitive hypertensive rats.Hypertension research : official journal of the Japanese Society of Hypertension · 2019Article
- Renal disease pathophysiology and treatment: contributions from the rat.Disease models & mechanisms · 2016Review
- Third-generation Mineralocorticoid Receptor Antagonists: Why Do We Need a Fourth?Journal of cardiovascular pharmacology · 2016Review
- Genome-wide analysis of murine renal distal convoluted tubular cells for the target genes of mineralocorticoid receptor.Biochemical and biophysical research communications · 2014Article
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The mineralocorticoid receptor (MR) is a member of the steroid-responsive nuclear receptor family. Currently, in addition to its classical role in fluid homeostasis, attention has been focused on the pro-proteinuric and pro-inflammatory effects of MR in renal and cardiovascular diseases. Since proteinuria has been shown to be an important factor in the prognosis of patients with chronic kidney disease (CKD) [according to the newest Japanese Society of Nephrology and Kidney Disease: Improving Global Outcomes (KDIGO) guidelines for the treatment of CKD], it is worth discussing the role of MR in the progression of proteinuric CKD and the possible association with podocyte injury. Rac1, a Rho-GTPase family protein, is known for its role in the regulation of the cytoskeleton. We discovered the role of active Rac1 in amplifying MR activation in one of our studies and then continued to study how the Rac1-MR pathway contributes to the progression of kidney diseases. We then discovered the harmful effects of the activation of the Rac1-MR pathway in response to salt loading in the kidney for proteinuric kidney diseases of various animal models with salt-sensitive hypertension, such as Dahl salt-sensitive rats, RhoGDIα-knockout mice, angiotensin II-overproducing mice, and aldosterone-infused rats. In this review, we have introduced recent findings that suggest the contribution of MR activation to kidney diseases and the role of the Rac1-MR pathway in kidney injury associated with salt-sensitive hypertension and proteinuria. Thus, the Rac1-MR pathway is a potential therapeutic target in patients with proteinuric CKD.
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