ArticleKidney international2016
Deletion of mineralocorticoid receptors in smooth muscle cells blunts renal vascular resistance following acute cyclosporine administration.
Article in Kidney international, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed, 60 citations in OpenAlex.
- Safety of Eplerenone for Kidney-Transplant Recipients with Impaired Renal Function and Receiving Cyclosporine A.PloS one · 2016Trial
- Article
- Mineralocorticoid receptor activation contributes to intestinal fibrosis through neutrophil gelatinase-associated lipocalin in preclinical models.Nature communications · 2025Article
- Mineralocorticoid receptor blockage in kidney transplantation: too much of a good thing or not?International urology and nephrology · 2025Review
- Mineralocorticoid receptor antagonism for non-diabetic kidney disease.Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association · 2025Review
- Recent Advances and Perspectives on the Use of Mineralocorticoid Receptor Antagonists for the Treatment of Hypertension and Chronic Kidney Disease: A Review.Biomedicines · 2024Review
- Mineralocorticoid Receptors in Vascular Smooth Muscle: Blood Pressure and Beyond.Hypertension (Dallas, Tex. : 1979) · 2024Review
- The Mineralocorticoid Receptor in the Vasculature: Friend or Foe?Annual review of physiology · 2024Review
- Extra-adrenal aldosterone: a mini review focusing on the physiology and pathophysiology of intrarenal aldosterone.Endocrine · 2024Review
- Calcineurin Is a Universal Regulator of Vessel Function-Focus on Vascular Smooth Muscle Cells.Cells · 2023Review
- The Mineralocorticoid Receptor on Smooth Muscle Cells Promotes Tacrolimus-Induced Renal Injury in Mice.Pharmaceutics · 2023Article
- Emerging vascular cell-specific roles for mineralocorticoid receptor: implications for understanding sex differences in cardiovascular disease.American journal of physiology. Cell physiology · 2023Review
- Biglycan Is a Novel Mineralocorticoid Receptor Target Involved in Aldosterone/Salt-Induced Glomerular Injury.International journal of molecular sciences · 2022Article
- Nonepithelial mineralocorticoid receptor activation as a determinant of kidney disease.Kidney international supplements · 2022Review
- Neutrophil gelatinase-associated lipocalin as an immunomodulator in endocrine hypertension.Frontiers in endocrinology · 2022Review
- Oxidized Albumin as a Mediator of Kidney Disease.Antioxidants (Basel, Switzerland) · 2021Review
- Mineralocorticoid Receptor in Smooth Muscle Contributes to Pressure Overload-Induced Heart Failure.Circulation. Heart failure · 2021Article
- The Role of Neutrophils in Hypertension.International journal of molecular sciences · 2020Review
- Aldosterone and the mineralocorticoid receptor in renal injury: A potential therapeutic target in feline chronic kidney disease.Journal of veterinary pharmacology and therapeutics · 2020Review
- Approach and Management of Hypertension After Kidney Transplantation.Frontiers in medicine · 2020Review
Corrections and comments
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Authors and funding
12 authors at 7 institutions in 3 countries.
Funding
Abstract
Calcineurin inhibitors such as cyclosporine A (CsA) are still commonly used after renal transplantation, despite CsA--induced nephrotoxicity (CIN), which is partly related to vasoactive mechanisms. The mineralocorticoid receptor (MR) is now recognized as a key player in the control of vascular tone, and both endothelial cell- and vascular smooth muscle cell (SMC)-MR modulate the vasoactive responses to vasodilators and vasoconstrictors. Here we tested whether vascular MR is involved in renal hemodynamic changes induced by CsA. The relative contribution of vascular MR in acute CsA treatment was evaluated using mouse models with targeted deletion of MR in endothelial cell or SMC. Results indicate that MR expressed in SMC, but not in endothelium, contributes to the increase of plasma urea and creatinine, the appearance of isometric tubular vacuolization, and overexpression of a kidney injury biomarker (neutrophil gelatinase--associated lipocalin) after CsA treatment. Inactivation of MR in SMC blunted CsA--induced phosphorylation of contractile proteins. Finally, the in vivo increase of renal vascular resistance induced by CsA was blunted when MR was deleted from SMC cells, and this was associated with decreased L-type Ca2D channel activity. Thus, our study provides new insights into the role of vascular MR in renal hemodynamics during acute CIN, and provides rationale for clinical studies of MR antagonism to manage the side effects of calcineurin inhibitors.
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Registered trials
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