ReviewFrontiers in pharmacology2018
GRK5 - A Functional Bridge Between Cardiovascular and Neurodegenerative Disorders.
Review in Frontiers in pharmacology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 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
18 citing papers in PubMed.
- Comparative Phosphoproteomic Profiling and Network-based Interactome Analysis of GRK5 and GRK6.Cell biochemistry and biophysics · 2026Article
- Potential Cardioprotective Effect of a GRK5 Inhibitor Against NF-κB-Mediated Inflammation in an Animal Model of Isoproterenol-Induced Myocardial Infarction.International journal of molecular sciences · 2025Article
- P-Rex1 limits the agonist-induced internalization of GPCRs independently of its Rac-GEF activity.Cell reports · 2025Article
- Global functional genomics reveals GRK5 as a cystic fibrosis therapeutic target synergistic with current modulators.iScience · 2025Article
- Genomic and ancestral variations linked to the development of post-acute sequelae of SARS-CoV-2 infection in Indian populations.Frontiers in genetics · 2025Article
- Article
- Uncovering conserved networks and global conformational changes in G protein-coupled receptor kinases.Computational and structural biotechnology journal · 2024Article
- G protein-coupled receptor kinase 5 regulates thrombin signaling in platelets.Research and practice in thrombosis and haemostasis · 2024Article
- Machine Learning Analysis of Alzheimer's Disease Single-Cell RNA-Sequencing Data across Cortex and Hippocampus Regions.Current issues in molecular biology · 2023Article
- Type 2 diabetes susceptibility gene GRK5 regulates physiological pancreatic β-cell proliferation via phosphorylation of HDAC5.iScience · 2023Article
- G protein-coupled receptor signaling: transducers and effectors.American journal of physiology. Cell physiology · 2022Review
- GRK5 Deficiency Causes Mild Cognitive Impairment due to Alzheimer's Disease.Journal of Alzheimer's disease : JAD · 2022Review
- The genetics of cardiac failure: Role of a G protein-coupled receptor polymorphism in therapeutic response in an Indian population.Journal of clinical and translational research · 2021Article
- Targeting GRK5 for Treating Chronic Degenerative Diseases.International journal of molecular sciences · 2021Review
- The Microbiota-Gut-Brain Axis-Heart Shunt Part II: Prosaic Foods and the Brain-Heart Connection in Alzheimer Disease.Microorganisms · 2020Article
- Structure-Based Design of Selective, Covalent G Protein-Coupled Receptor Kinase 5 Inhibitors.ACS medicinal chemistry letters · 2019Article
- G Protein-Coupled Receptor Systems and Their Role in Cellular Senescence.Computational and structural biotechnology journal · 2019Review
- GPCR Signaling Regulation: The Role of GRKs and Arrestins.Frontiers in pharmacology · 2019Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Complex aging-triggered disorders are multifactorial programs that comprise a myriad of alterations in interconnected protein networks over a broad range of tissues. It is evident that rather than being randomly organized events, pathophysiologies that possess a strong aging component such as cardiovascular diseases (hypertensions, atherosclerosis, and vascular stiffening) and neurodegenerative conditions (dementia, Alzheimer's disease, mild cognitive impairment, Parkinson's disease), in essence represent a subtly modified version of the intricate molecular programs already in place for normal aging. To control such multidimensional activities there are layers of trophic protein control across these networks mediated by so-called "keystone" proteins. We propose that these "keystones" coordinate and interconnect multiple signaling pathways to control whole somatic activities such as aging-related disease etiology. Given its ability to control multiple receptor sensitivities and its broad protein-protein interactomic nature, we propose that G protein coupled receptor kinase 5 (GRK5) represents one of these key network controllers. Considerable data has emerged, suggesting that GRK5 acts as a bridging factor, allowing signaling regulation in pathophysiological settings to control the connectivity between both the cardiovascular and neurophysiological complications of aging.
Indexed as
Identifiers
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.