ArticleAmerican journal of transplantation : official journal of the American Society of Transplantation and the American Society of Transplant Surgeons2010
RGS4 controls renal blood flow and inhibits cyclosporine-mediated nephrotoxicity.
Article in American journal of transplantation : official journal of the American Society of Transplantation and the American Society of Transplant Surgeons, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 31 citations in OpenAlex.
- Hydralazine inhibits cysteamine dioxygenase to treat preeclampsia and senesce glioblastoma.Science advances · 2025Article
- Hydralazine inhibits cysteamine dioxygenase to treat preeclampsia and senesce glioblastoma.bioRxiv : the preprint server for biology · 2024Article
- Cardiac RGS Proteins in Human Heart Failure and Atrial Fibrillation: Focus on RGS4.International journal of molecular sciences · 2023Review
- Regulators of G protein signaling in cardiovascular function during pregnancy.Physiological genomics · 2018Review
- Human vascular progenitor cells derived from renal arteries are endothelial-like and assist in the repair of injured renal capillary networks.Kidney international · 2017Article
- Deletion of mineralocorticoid receptors in smooth muscle cells blunts renal vascular resistance following acute cyclosporine administration.Kidney international · 2016Article
- RGS4 inhibits angiotensin II signaling and macrophage localization during renal reperfusion injury independent of vasospasm.Kidney international · 2015Article
- Selective clinical and immune response of the oligoclonal autoreactive T cells in Omenn patients after cyclosporin A treatment.Clinical and experimental immunology · 2012Article
- Delayed graft function in the kidney transplant.American journal of transplantation : official journal of the American Society of Transplantation and the American Society of Transplant Surgeons · 2011Review
- RGS4, a GTPase activator, improves renal function in ischemia-reperfusion injury.Kidney international · 2011Article
- Novel insights into the function of β-cell M3 muscarinic acetylcholine receptors: therapeutic implications.Trends in endocrinology and metabolism: TEM · 2011Review
- RGS4 is a negative regulator of insulin release from pancreatic beta-cells in vitro and in vivo.Proceedings of the National Academy of Sciences of the United States of America · 2010Article
- The therapeutic potential of targeting cardiac RGS4.Therapeutic advances in cardiovascular diseaseReview
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 2 countries.
Funding
Abstract
Calcineurin inhibitors (CNI) are powerful immunomodulatory agents that produce marked renal dysfunction due in part to endothelin-1-mediated reductions in renal blood flow. Ligand-stimulated Gq protein signaling promotes the contraction of smooth muscle cells via phospholipase Cbeta-mediated stimulation of cytosolic calcium release. RGS4 is a GTPase activating protein that promotes the deactivation of Gq and Gi family members. To investigate the role of G protein-mediated signaling in the pathogenesis of CNI-mediated renal injury, we used mice deficient for RGS4 (rgs4(-/-)). Compared to congenic wild type control animals, rgs4(-/-) mice were intolerant of the CNI, cyclosporine (CyA), rapidly developing fatal renal failure. Rgs4(-/-) mice exhibited markedly reduced renal blood flow after CyA treatment when compared to congenic wild type control mice as measured by magnetic resonance imaging (MRI). Hypoperfusion was reversed by coadministration of CyA with the endothelin antagonist, bosentan. The MAPK/ERK pathway was activated by cyclosporine administration and was inhibited by cotreatment with bosentan. These results show that endothelin-1-mediated Gq protein signaling plays a key role in the pathogenesis of vasoconstrictive renal injury and that RGS4 antagonizes the deleterious effects of excess endothelin receptor activation in the kidney.
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Registered trials
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