ReviewBiochimica et biophysica acta. Molecular basis of disease2017
Targeting GPCR-Gβγ-GRK2 signaling as a novel strategy for treating cardiorenal pathologies.
Review in Biochimica et biophysica acta. Molecular basis of disease, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
14 citing papers in PubMed, 22 citations in OpenAlex.
- Current Perspectives on the NF-κB Signaling Axis as a Potential Pharmacological Target in Cardiorenal Syndrome.Drug design, development and therapy · 2025Review
- 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
- Stress-induced differential gene expression in cardiac tissue.Scientific reports · 2021Article
- 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
- Single-Cell Profiling of AKI in a Murine Model Reveals Novel Transcriptional Signatures, Profibrotic Phenotype, and Epithelial-to-Stromal Crosstalk.Journal of the American Society of Nephrology : JASN · 2020Article
- Modulation of polycystic kidney disease by G-protein coupled receptors and cyclic AMP signaling.Cellular signalling · 2020Review
- β-Adrenergic receptor, an essential target in cardiovascular diseases.Heart failure reviews · 2020Review
- Angiotensin Receptors Heterodimerization and Trafficking: How Much Do They Influence Their Biological Function?Frontiers in pharmacology · 2020Review
- G Protein-Coupled Receptor Kinase 2 (GRK2) as a Potential Therapeutic Target in Cardiovascular and Metabolic Diseases.Frontiers in pharmacology · 2019Review
- Gpr97 Exacerbates AKI by Mediating Sema3A Signaling.Journal of the American Society of Nephrology : JASN · 2018Article
- Insulin receptor substrate signaling controls cardiac energy metabolism and heart failure.The Journal of endocrinology · 2017Review
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
The pathologic crosstalk between the heart and kidney is known as cardiorenal syndrome (CRS). While the specific mechanisms underlying this crosstalk remain poorly understood, CRS is associated with exacerbated dysfunction of either or both organs and reduced survival. Maladaptive fibrotic remodeling is a key component of both heart and kidney failure pathogenesis and progression. G-protein coupled receptor (GPCR) signaling is a crucial regulator of cardiovascular and renal function. Chronic/pathologic GPCR signaling elicits the interaction of the G-protein Gβγ subunit with GPCR kinase 2 (GRK2), targeting the receptor for internalization, scaffolding to pathologic signals, and receptor degradation. Targeting this pathologic Gβγ-GRK2 interaction has been suggested as a possible strategy for the treatment of HF. In the current review, we discuss recent updates in understanding the role of GPCR-Gβγ-GRK2 signaling as a crucial mediator of maladaptive organ remodeling detected in HF and kidney dysfunction, with specific attention to small molecule-mediated inhibition of pathologic Gβγ-GRK2 interactions. Further, we explore the potential of GPCR-Gβγ-GRK2 signaling as a possible therapeutic target for cardiorenal pathologies.
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What Socratic holds
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.