ArticleJournal of cellular and molecular medicine2016
Novel EGFR inhibitors attenuate cardiac hypertrophy induced by angiotensin II.
Article in Journal of cellular and molecular medicine, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
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Who cites it
35 citing papers in PubMed, 67 citations in OpenAlex.
- Pioglitazone Mitigates Arsenic-Induced Cardiotoxicity via Lipid Metabolism: Network Pharmacology and Molecular Docking Approach.Cardiovascular toxicology · 2026Article
- SNX16 aggravates AngII-induced cardiac hypertrophy in mice via EGFR transactivation.Communications biology · 2025Article
- Self-assembled extracellular matrix-lipid nanoparticle composite for site-specific siRNA delivery to improve cardiac repair post-myocardial infarction.Materials today. Bio · 2025Article
- The role of deubiquitinases in cardiac disease.Expert reviews in molecular medicine · 2024Review
- DNMT3A clonal hematopoiesis-driver mutations induce cardiac fibrosis by paracrine activation of fibroblasts.Nature communications · 2024Article
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- Role of c-Src and reactive oxygen species in cardiovascular diseases.Molecular genetics and genomics : MGG · 2023Review
- Signaling network model of cardiomyocyte morphological changes in familial cardiomyopathy.Journal of molecular and cellular cardiology · 2023Article
- Alteration in tyrosine phosphorylation of cardiac proteome and EGFR pathway contribute to hypertrophic cardiomyopathy.Communications biology · 2022Article
- Loss of Amphiregulin drives inflammation and endothelial apoptosis in pulmonary hypertension.Life science alliance · 2022Article
- A Bioinformatics Investigation into the Pharmacological Mechanisms of Sodium-Glucose Co-transporter 2 Inhibitors in Diabetes Mellitus and Heart Failure Based on Network Pharmacology.Cardiovascular drugs and therapy · 2022Article
- Article
- 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
- The Roles of S100A4 and the EGF/EGFR Signaling Axis in Pulmonary Hypertension with Right Ventricular Hypertrophy.Biology · 2022Article
- SchizoGoogLeNet: The GoogLeNet-Based Deep Feature Extraction Design for Automatic Detection of Schizophrenia.Computational intelligence and neuroscience · 2022Article
- Reversion inducing cysteine rich protein with Kazal motifs and cardiovascular diseases: The RECKlessness of adverse remodeling.Cellular signalling · 2021Review
- The Impact of microRNAs in Renin-Angiotensin-System-Induced Cardiac Remodelling.International journal of molecular sciences · 2021Review
- The Role of Epidermal Growth Factor Receptor Family of Receptor Tyrosine Kinases in Mediating Diabetes-Induced Cardiovascular Complications.Frontiers in pharmacology · 2021Review
- An Insight on Multicentric Signaling of Angiotensin II in Cardiovascular system: A Recent Update.Frontiers in pharmacology · 2021Review
- The Role of iRhom2 in Metabolic and Cardiovascular-Related Disorders.Frontiers in cardiovascular medicine · 2020Review
Corrections and comments
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Authors and funding
10 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cardiac hypertrophy is an important risk factor for heart failure. Epidermal growth factor receptor (EGFR) has been found to play a role in the pathogenesis of various cardiovascular diseases. The aim of this current study was to examine the role of EGFR in angiotensin II (Ang II)-induced cardiac hypertrophy and identify the underlying molecular mechanisms. In this study, we observed that both Ang II and EGF could increase the phospohorylation of EGFR and protein kinase B (AKT)/extracellular signal-regulated kinase (ERK), and then induce cell hypertrophy in H9c2 cells. Both pharmacological inhibitors and genetic silencing significantly reduced Ang II-induced EGFR signalling pathway activation, hypertrophic marker overexpression, and cell hypertrophy. In addition, our results showed that Ang II-induced EGFR activation is mediated by c-Src phosphorylation. In vivo, Ang II treatment significantly led to cardiac remodelling including cardiac hypertrophy, disorganization and fibrosis, accompanied by the activation of EGFR signalling pathway in the heart tissues, while all these molecular and pathological alterations were attenuated by the oral administration with EGFR inhibitors. In conclusion, the c-Src-dependent EGFR activation may play an important role in Ang II-induced cardiac hypertrophy, and inhibition of EGFR by specific molecules may be an effective strategy for the treatment of Ang II-associated cardiac diseases.
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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.