ArticleJournal of the American Society of Nephrology : JASN2014
Myeloid mineralocorticoid receptor activation contributes to progressive kidney disease.
Article in Journal of the American Society of Nephrology : JASN, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
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Who cites it
36 citing papers in PubMed.
- Deficiency of mineralocorticoid receptor signalling in myeloid cells protects cardiac and kidney function in hypertensive diabetic mice.Clinical science (London, England : 1979) · 2025Article
- Mineralocorticoid receptor antagonists promote renal immunosenescence.International urology and nephrology · 2025Review
- Cardiovascular-Kidney-Metabolic Effects: Steroidal and Nonsteroidal Mineralocorticoid Receptor Antagonists.Reviews in cardiovascular medicine · 2025Review
- Clinical implications of mineralocorticoid receptor overactivation.Clinical kidney journal · 2025Review
- Renal macrophages and NLRP3 inflammasomes in kidney diseases and therapeutics.Cell death discovery · 2024Review
- The role of a novel mineralocorticoid receptor antagonist, finerenone, in chronic kidney disease: mechanisms and clinical advances.Clinical and experimental nephrology · 2024Review
- Biomarkers to Guide Medical Therapy in Primary Aldosteronism.Endocrine reviews · 2024Review
- Cardiorenal benefits of finerenone: protecting kidney and heart.Annals of medicine · 2023Review
- Aldosterone: Essential for Life but Damaging to the Vascular Endothelium.Biomolecules · 2023Review
- Effects of Finerenone on Cardiovascular and Chronic Kidney Diseases: A New Weapon against Cardiorenal Morbidity and Mortality-A Comprehensive Review.Journal of cardiovascular development and disease · 2023Review
- Mineralocorticoid Receptor Antagonists for Preventing Chronic Kidney Disease Progression: Current Evidence and Future Challenges.International journal of molecular sciences · 2023Review
- Overview of the safety, efficiency, and potential mechanisms of finerenone for diabetic kidney diseases.Frontiers in endocrinology · 2023Review
- Nonsteroidal Mineralocorticoid Receptor Antagonism by Finerenone-Translational Aspects and Clinical Perspectives across Multiple Organ Systems.International journal of molecular sciences · 2022Review
- Biglycan Is a Novel Mineralocorticoid Receptor Target Involved in Aldosterone/Salt-Induced Glomerular Injury.International journal of molecular sciences · 2022Article
- Investigating new treatment opportunities for patients with chronic kidney disease in type 2 diabetes: the role of finerenone.Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association · 2022Article
- Nonepithelial mineralocorticoid receptor activation as a determinant of kidney disease.Kidney international supplements · 2022Review
- Role of Finerenone in the Treatment of Diabetic Kidney Disease: Patient Selection and Clinical Perspectives.Therapeutics and clinical risk management · 2022Review
- A Glimpse of Inflammation and Anti-Inflammation Therapy in Diabetic Kidney Disease.Frontiers in physiology · 2022Review
- Mineralocorticoid receptor antagonists in diabetic kidney disease - mechanistic and therapeutic effects.Nature reviews. Nephrology · 2022Review
- Myeloid Mineralocorticoid Receptor Transcriptionally Regulates P-Selectin Glycoprotein Ligand-1 and Promotes Monocyte Trafficking and Atherosclerosis.Arteriosclerosis, thrombosis, and vascular biology · 2021Article
Corrections and comments
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Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Clinical and experimental studies have shown that mineralocorticoid receptor (MR) antagonists substantially reduce kidney injury. However, the specific cellular targets and mechanisms by which MR antagonists protect against kidney injury must be identified. We used conditional gene deletion of MR signaling in myeloid cells (MR(flox/flox) LysM(Cre) mice; MyMRKO) or podocytes (MR(flox/flox) Pod(Cre) mice; PodMRKO) to establish the role of MR in these cell types in the development of mouse GN. Accelerated anti-glomerular basement membrane GN was examined in groups of mice: MyMRKO, PodMRKO, wild-type (WT) littermates, and WT mice receiving eplerenone (100 mg/kg twice a day; EPL-treated). At day 15 of disease, WT mice had glomerular crescents (37%±5%), severe proteinuria, and a 6-fold increase in serum cystatin-C. MyMRKO, PodMRKO, and EPL-treated mice with GN displayed proteinuria similar to that in these disease controls. However, MyMRKO and EPL-treated groups had a 35% reduction in serum cystatin-C levels and reduced crescent numbers compared with WT mice, whereas PodMRKO mice were not protected. The protection observed in MyMRKO mice appeared to result predominantly from reduced recruitment of macrophages and neutrophils into the inflamed kidney. Suppression of kidney leukocyte accumulation in MyMRKO mice correlated with reductions in gene expression of proinflammatory molecules (TNF-α, inducible nitric oxide synthase, chemokine (C-C motif) ligand 2, matrix metalloproteinase-12), tubular damage, and renal fibrosis and was similar in EPL-treated mice. In conclusion, MR signaling in myeloid cells, but not podocytes, contributes to the progression of renal injury in mouse GN, and myeloid deficiency of MR provides protection similar to eplerenone in this disease.
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