ArticleHypertension (Dallas, Tex. : 1979)2014
Role of GRK4 in the regulation of arterial AT1 receptor in hypertension.
Article in Hypertension (Dallas, Tex. : 1979), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
33 citing papers in PubMed, 42 citations in OpenAlex.
- Genetic evidence links hypertension to accelerated brain aging.Biogerontology · 2026Article
- Role of G-protein-coupled receptor kinase 4 on the dysfunction of renal Mas receptor in hypertension.PloS one · 2025Article
- Methylation Status at DMRs of C14MC and C19MC in Spermatozoa and Chorionic Villi of Individuals Experiencing Recurrent Spontaneous Abortions.Reproductive sciences (Thousand Oaks, Calif.) · 2025Article
- G protein-coupled receptor kinases in hypertension: physiology, pathogenesis, and therapeutic targets.Hypertension research : official journal of the Japanese Society of Hypertension · 2024Review
- Selenium deficiency causes hypertension by increasing renal ATFree radical biology & medicine · 2023Article
- Downregulation of G protein-coupled receptor kinase 4 protects against kidney ischemia-reperfusion injury.Kidney international · 2023Article
- Comprehensive insights in GRK4 and hypertension: From mechanisms to potential therapeutics.Pharmacology & therapeutics · 2022Review
- G-protein-coupled receptor kinase 4 causes renal angiotensin II type 2 receptor dysfunction by increasing its phosphorylation.Clinical science (London, England : 1979) · 2022Article
- Double life: How GRK2 and β-arrestin signaling participate in diseases.Cellular signalling · 2022Review
- Paternal long-term PM2.5 exposure causes hypertension via increased renal AT1R expression and function in male offspring.Clinical science (London, England : 1979) · 2021Article
- Genetic variants of GRK4 influence circadian rhythm of blood pressure and response to candesartan in hypertensive patients.Clinical and experimental hypertension (New York, N.Y. : 1993) · 2021Article
- Increased ATHypertension research : official journal of the Japanese Society of Hypertension · 2021Article
- The GRKs Reactome: Role in Cell Biology and Pathology.International journal of molecular sciences · 2021Review
- Role of GRK2 in Trophoblast Necroptosis and Spiral Artery Remodeling: Implications for Preeclampsia Pathogenesis.Frontiers in cell and developmental biology · 2021Article
- GRK4-mediated adiponectin receptor-1 phosphorylative desensitization as a novel mechanism of reduced renal sodium excretion in hypertension.Clinical science (London, England : 1979) · 2020Article
- Role of GRK4 in the regulation of the renal ETB receptor in hypertension.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2020Article
- Angiotensin Receptors Heterodimerization and Trafficking: How Much Do They Influence Their Biological Function?Frontiers in pharmacology · 2020Review
- Small-Molecule G Protein-Coupled Receptor Kinase Inhibitors Attenuate G Protein-Coupled Receptor Kinase 2-Mediated Desensitization of Vasoconstrictor-Induced Arterial Contractions.Molecular pharmacology · 2018Article
- The Role of G Protein-coupled Receptor Kinases in Cancer.International journal of biological sciences · 2018Review
- Activation of angiotensin II type 1 receptors increases DHypertension research : official journal of the Japanese Society of Hypertension · 2017Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
13 authors at 2 institutions in 1 country.
Funding
Abstract
G-protein-coupled receptor kinase 4 (GRK4) gene variants, via impairment of renal dopamine receptor and enhancement of renin-angiotensin system functions, cause sodium retention and increase blood pressure. Whether GRK4 and the angiotensin type 1 receptor (AT(1)R) interact in the aorta is not known. We report that GRK4 is expressed in vascular smooth muscle cells of the aorta. Heterologous expression of the GRK4γ variant 142V in A10 cells increased AT(1)R protein expression and AT(1)R-mediated increase in intracellular calcium concentration. The increase in AT(1)R expression was related to an increase in AT(1)R mRNA expression via the NF-κB pathway. As compared with control, cells expressing GRK4γ 142V had greater NF-κB activity with more NF-κB bound to the AT(1)R promoter. The increased AT(1)R expression in cells expressing GRK4γ 142V was also associated with decreased AT(1)R degradation, which may be ascribed to lower AT(1)R phosphorylation. There was a direct interaction between GRK4γ and AT(1)R that was decreased by GRK4γ 142V. The regulation of AT(1)R expression by GRK4γ 142V in A10 cells was confirmed in GRK4γ 142V transgenic mice; AT(1)R expression was higher in the aorta of GRK4γ 142V transgenic mice than control GRK4γ wild-type mice. Angiotensin II-mediated vasoconstriction of the aorta was also higher in GRK4γ 142V than in wild-type transgenic mice. This study provides a mechanism by which GRK4, via regulation of arterial AT(1)R expression and function, participates in the pathogenesis of conduit vessel abnormalities in hypertension.
Indexed as
Identifiers
What OpenQuestion 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 OpenQuestion graph.