ArticleJournal of the American Society of Nephrology : JASN2017
G Protein-Coupled Receptor-G-Protein βγ-Subunit Signaling Mediates Renal Dysfunction and Fibrosis in Heart Failure.
Article in Journal of the American Society of Nephrology : JASN, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed, 49 citations in OpenAlex.
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- Low Temperature Plasma Jet Treatment Promotes Skin Wound Healing by Enhancing Cell Proliferation via the PI3K-AKT and AMPK Pathways.International wound journal · 2025Article
- G protein-coupled receptor-mediated renal fibrosis: a key focus on kidney disease drug development.Frontiers in pharmacology · 2025Review
- The roles of G protein-coupled receptor kinase 2 in renal diseases.Journal of cellular and molecular medicine · 2024Review
- Paeoniflorin-6'O-benzene sulfonate suppresses fibroblast-like synoviocytes proliferation and migration in rheumatoid arthritis through regulating GRK2-Gβγ interaction.Experimental and therapeutic medicine · 2022Article
- Early Gβγ-GRK2 Inhibition Ameliorates Osteoarthritis Development by Simultaneous Anti-Inflammatory and Chondroprotective Effects.International journal of molecular sciences · 2022Article
- Targeting GPCRs to treat cardiac fibrosis.Frontiers in cardiovascular medicine · 2022Review
- Toward Human Models of Cardiorenal SyndromeFrontiers in cardiovascular medicine · 2022Review
- Mildly Increased Renin Expression in the Absence of Kidney Injury in the Murine Transverse Aortic Constriction Model.Frontiers in pharmacology · 2021Article
- G Protein-Coupled Receptor Kinase 2 as Novel Therapeutic Target in Fibrotic Diseases.Frontiers in immunology · 2021Review
- Range of adiposity and cardiorenal syndrome.World journal of diabetes · 2020Review
- An improved clear cell renal cell carcinoma stage prediction model based on gene sets.BMC bioinformatics · 2020Article
- Chromogranin A pathway: from pathogenic molecule to renal disease.Journal of hypertension · 2020Article
- Cannabinoid Receptor 2 (CBACS pharmacology & translational science · 2019Article
- G protein-coupled receptor kinases as therapeutic targets in the heart.Nature reviews. Cardiology · 2019Review
- Molecular Mechanisms of Kidney Injury and Repair in Arterial Hypertension.International journal of molecular sciences · 2019Review
- Distinct Phenotypes Induced by Three Degrees of Transverse Aortic Constriction in Mice.Scientific reports · 2019Article
- Design, Synthesis, and Actions of an Innovative Bispecific Designer Peptide.Hypertension (Dallas, Tex. : 1979) · 2019Article
- Wnt/β-catenin signaling mediates both heart and kidney injury in type 2 cardiorenal syndrome.Kidney international · 2019Article
- Hydrogen Sulfide Attenuates Renin Angiotensin and Aldosterone Pathological Signaling to Preserve Kidney Function and Improve Exercise Tolerance in Heart Failure.JACC. Basic to translational science · 2018Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
Abstract
Development of CKD secondary to chronic heart failure (CHF), known as cardiorenal syndrome type 2 (CRS2), clinically associates with organ failure and reduced survival. Heart and kidney damage in CRS2 results predominantly from chronic stimulation of G protein-coupled receptors (GPCRs), including adrenergic and endothelin (ET) receptors, after elevated neurohormonal signaling of the sympathetic nervous system and the downstream ET system, respectively. Although we and others have shown that chronic GPCR stimulation and the consequent upregulated interaction between the G-protein βγ-subunit (Gβγ), GPCR-kinase 2, and β-arrestin are central to various cardiovascular diseases, the role of such alterations in kidney diseases remains largely unknown. We investigated the possible salutary effect of renal GPCR-Gβγ inhibition in CKD developed in a clinically relevant murine model of nonischemic hypertrophic CHF, transverse aortic constriction (TAC). By 12 weeks after TAC, mice developed CKD secondary to CHF associated with elevated renal GPCR-Gβγ signaling and ET system expression. Notably, systemic pharmacologic Gβγ inhibition by gallein, which we previously showed alleviates CHF in this model, attenuated these pathologic renal changes. To investigate a direct effect of gallein on the kidney, we used a bilateral ischemia-reperfusion AKI mouse model, in which gallein attenuated renal dysfunction, tissue damage, fibrosis, inflammation, and ET system activation. Furthermore, in vitro studies showed a key role for ET receptor-Gβγ signaling in pathologic fibroblast activation. Overall, our data support a direct role for GPCR-Gβγ in AKI and suggest GPCR-Gβγ inhibition as a novel therapeutic approach for treating CRS2 and AKI.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.