ReviewJournal of cardiovascular pharmacology2017
Cardiac GPCR-Mediated EGFR Transactivation: Impact and Therapeutic Implications.
Review in Journal of cardiovascular pharmacology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 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
21 citing papers in PubMed, 30 citations in OpenAlex.
- Cycloastragenol Attenuates Angiotensin II-Induced Cardiac Remodeling in Association with Enhanced EGFR Lysosomal Turnover and Changes in MAPK Signaling and Autophagy.Pharmaceuticals (Basel, Switzerland) · 2026Article
- High-throughput screening of EGFR/CaJournal of pharmaceutical analysis · 2026Article
- The regenerative wound healing effects and molecular mechanism of Isaria cicadae Miquel rice fermentation extract.Applied microbiology and biotechnology · 2025Article
- Transactivation of the EGF receptor as a novel desensitization mechanism for G protein-coupled receptors, illustrated by dopamine D2-like and βCellular & molecular biology letters · 2024Article
- Direct GPCR-EGFR interaction enables synergistic membrane-to-nucleus information transfer.Cellular and molecular life sciences : CMLS · 2024Article
- Exploring the pathways of drug repurposing and Panax ginseng treatment mechanisms in chronic heart failure: a disease module analysis perspective.Scientific reports · 2024Article
- Myeloid cell-specific deletion of epidermal growth factor receptor aggravates acute cardiac injury.Clinical science (London, England : 1979) · 2023Article
- Formyl-peptide receptor 2 signalling triggers aerobic metabolism of glucose through Nox2-dependent modulation of pyruvate dehydrogenase activity.Open biology · 2023Article
- TRAIL and its receptors in cardiac diseases.Frontiers in physiology · 2023Review
- Evolution of the ErbB gene family and analysis of regulators ofNeural regeneration research · 2022Article
- Serodolin, a β-arrestin-biased ligand of 5-HTProceedings of the National Academy of Sciences of the United States of America · 2022Article
- EMT-mediated regulation of CXCL1/5 for resistance to anti-EGFR therapy in colorectal cancer.Oncogene · 2022Article
- Epidermal growth factor receptor-dependent maintenance of cardiac contractility.Cardiovascular research · 2022Article
- Zinc finger and BTB domain-containing protein 20 aggravates angiotensin II-induced cardiac remodeling via the EGFR-AKT pathway.Journal of molecular medicine (Berlin, Germany) · 2022Article
- α7 Nicotinic acetylcholine receptor mediates right ventricular fibrosis and diastolic dysfunction in pulmonary hypertension.JCI insight · 2021Article
- Transactivation of G protein-coupled receptors (GPCRs) and receptor tyrosine kinases (RTKs): Recent insights using luminescence and fluorescence technologies.Current opinion in endocrine and metabolic research · 2021Review
- Context-specific network modeling identifies new crosstalk in β-adrenergic cardiac hypertrophy.PLoS computational biology · 2020Article
- β2-Adrenergic Receptors Increase Cardiac Fibroblast Proliferation Through the Gαs/ERK1/2-Dependent Secretion of Interleukin-6.International journal of molecular sciences · 2020Article
- Death receptor 5 contributes to cardiomyocyte hypertrophy through epidermal growth factor receptor transactivation.Journal of molecular and cellular cardiology · 2019Article
- Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
G protein-coupled receptors (GPCRs) remain primary therapeutic targets for numerous cardiovascular disorders, including heart failure (HF), because of their influence on cardiac remodeling in response to elevated neurohormone signaling. GPCR blockers have proven to be beneficial in the treatment of HF by reducing chronic G protein activation and cardiac remodeling, thereby extending the lifespan of patients with HF. Unfortunately, this effect does not persist indefinitely, thus next-generation therapeutics aim to selectively block harmful GPCR-mediated pathways while simultaneously promoting beneficial signaling. Transactivation of epidermal growth factor receptor (EGFR) has been shown to be mediated by an expanding repertoire of GPCRs in the heart, and promotes cardiomyocyte survival, thus may offer a new avenue of HF therapeutics. However, GPCR-dependent EGFR transactivation has also been shown to regulate cardiac hypertrophy and fibrosis by different GPCRs and through distinct molecular mechanisms. Here, we discuss the mechanisms and impact of GPCR-mediated EGFR transactivation in the heart, focusing on angiotensin II, urotensin II, and β-adrenergic receptor systems, and highlight areas of research that will help us to determine whether this pathway can be engaged as future therapeutic strategy.
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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 OpenQuestion graph.