ArticleJournal of molecular and cellular cardiology2015
EGFR inhibition protects cardiac damage and remodeling through attenuating oxidative stress in STZ-induced diabetic mouse model.
Article in Journal of molecular and cellular cardiology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers, 1 of them a synthesis that pooled it.
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Who cites it
36 citing papers in PubMed, 1 synthesis or guideline pooled it, 65 citations in OpenAlex.
- Macrophage-associated kinase signaling in atherosclerosis - a systematic review.Cell communication and signaling : CCS · 2026Pooled it
- Malignant Transformation Risk in Patients With Oral Leukoplakia and Type 2 Diabetes Mellitus.International dental journal · 2026Article
- Association between Magnesium Depletion Score and Hypertension: Insights from a Large-Scale Population-Based Study and Bioinformatics Analysis.Biological trace element research · 2026Article
- Exploring the Protective Effect and Potential Mechanism of Acutumidine on Myocardial Ischemia based on "Compound-Target-Pathway" Network.Combinatorial chemistry & high throughput screening · 2026Article
- Portulaca oleracea-derived indoline amide ameliorates obesity and NAFLD in rats through Nrf2-dependent antioxidant and anti-inflammatory mechanisms.Scientific reports · 2025Article
- Potential Mechanism by which Eriodictyol Protects against Doxorubicininduced Cardiotoxicity based on Network Pharmacology, Molecular Docking, and Molecular Dynamics Simulation.Current computer-aided drug design · 2025Article
- Hypertrophic cardiomyopathy-associated mutations drive stromal activation via EGFR-mediated paracrine signaling.Science advances · 2024Article
- Hyperglycemia activates FGFR1Acta pharmaceutica Sinica. B · 2024Article
- Glucose upregulates amphiregulin in oral dysplastic keratinocytes: A potential role in diabetes-associated oral carcinogenesis.Journal of oral pathology & medicine : official publication of the International Association of Oral Pathologists and the American Academy of Oral Pathology · 2023Article
- Chemical Constituents and Hypoglycemic Mechanisms ofMolecules (Basel, Switzerland) · 2023Article
- The role of autophagy in cardiovascular disease: Cross-interference of signaling pathways and underlying therapeutic targets.Frontiers in cardiovascular medicine · 2023Review
- Review
- 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
- Bibliometric analysis of the inflammation in diabetic cardiomyopathy.Frontiers in cardiovascular medicine · 2022Article
- The Role of Epidermal Growth Factor Receptor Family of Receptor Tyrosine Kinases in Mediating Diabetes-Induced Cardiovascular Complications.Frontiers in pharmacology · 2021Review
- Basic Mechanisms of Diabetic Heart Disease.Circulation research · 2020Review
- MD2 activation by direct AGE interaction drives inflammatory diabetic cardiomyopathy.Nature communications · 2020Article
- Secreted Phospholipase ACells · 2020Article
- Inhibition of the ROS-EGFR Pathway Mediates the Protective Action of Nox1/4 Inhibitor GKT137831 against Hypertensive Cardiac Hypertrophy via Suppressing Cardiac Inflammation and Activation of Akt and ERK1/2.Mediators of inflammation · 2020Article
- Prokineticin 2 (PK2) Rescues Cardiomyocytes from High Glucose/High Palmitic Acid-Induced Damage by Regulating the AKT/GSK3Oxidative medicine and cellular longevity · 2020Article
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10 authors at 1 institution in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
Diabetes mellitus is strongly associated with cardiomyopathy. The underlying mechanisms for the development of diabetic cardiomyopathy are complex and not completely understood. Recent studies showed that epidermal growth factor receptors (EGFRs) are involved in diabetes-induced cardiac injury. However, the role of EGFR in the diabetic heart has yet to be confirmed. The aim of the present study is to further determine the role of EGRF in the pathogenesis of diabetic heart injury. The type 1 diabetic mice induced by streptozotocin were treated with EGFR inhibitors (AG1478 and 451) for 8 weeks, respectively. It was observed that diabetes induced phospohorylation of EGFR and AKT, increased cardiac ROS levels, and ultimately led to cardiac remodeling including cardiac hypertrophy, disorganization, apoptosis, and fibrosis, while all these molecular and pathological alterations were attenuated by the treatment with EGFR inhibitors. In vitro, either pharmacological inhibition of EGFR/AKT or sh-RNA silencing of EGFR significantly inhibited high concentration glucose (HG)-induced ROS generation and subsequently cell apoptosis in both cardiac H9C2 cells and primary rat cardiomyocytes, respectively. The ROS reduction by EGFR inhibitor was associated with the decreased NADPH oxidase activity and expression in H9c2 cells. HG-induced cardiomyocyte injuries were also reduced by NAC, an inhibitor of ROS. This study provides evidence that EGFR has a key role in the pathogenesis of STZ-induced diabetic cardiac damage and remodeling via ROS generation, and suggests that EGFR may be a potential target in treating diabetic cardiomyopathy.
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