ArticleHypertension (Dallas, Tex. : 1979)2012
A novel role for epidermal growth factor receptor tyrosine kinase and its downstream endoplasmic reticulum stress in cardiac damage and microvascular dysfunction in type 1 diabetes mellitus.
Article in Hypertension (Dallas, Tex. : 1979), 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers.
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Who cites it
54 citing papers in PubMed, 103 citations in OpenAlex.
- Integrative gene target mapping, RNA sequencing, in silico molecular docking, ADMET profiling and molecular dynamics simulation study of marine derived molecules for type 1 diabetes mellitus.Molecular diversity · 2026Article
- Endothelial CHOP as a central mechanism in renovascular hypertension-induced vascular endothelial dysfunction and cardiac fibrosis.Cellular and molecular life sciences : CMLS · 2025Article
- Hyperglycemia activates FGFR1Acta pharmaceutica Sinica. B · 2024Article
- Pharmacological Inhibition of Epidermal Growth Factor Receptor Prevents Intracranial Aneurysm Rupture by Reducing Endoplasmic Reticulum Stress.Hypertension (Dallas, Tex. : 1979) · 2024Article
- Article
- The amphiregulin/EGFR axis has limited contribution in controlling autoimmune diabetes.Scientific reports · 2023Article
- Effects of Tauroursodeoxycholic Acid and 4-Phenylbutyric Acid on Selenium Distribution in Mice Model with Type 1 Diabetes.Biological trace element research · 2023Article
- Plasmacytoid dendritic cells contribute to vascular endothelial dysfunction in type 2 diabetes.Frontiers in cardiovascular medicine · 2023Article
- Identification of candidate biomarkers and pathways associated with type 1 diabetes mellitus using bioinformatics analysis.Scientific reports · 2022Article
- Paradoxical effects of osteoprotegerin on vascular function: inhibiting inflammation while promoting oxidative stress?Clinical science (London, England : 1979) · 2022Article
- Disrupting Interleukin 12 Improves Microvascular Endothelial Function in Type 2 Diabetes Through ER Stress CHOP and Oxidative Stress Mechanisms.Diabetes, metabolic syndrome and obesity : targets and therapy · 2022Article
- Roles and Therapeutic Implications of Endoplasmic Reticulum Stress and Oxidative Stress in Cardiovascular Diseases.Antioxidants (Basel, Switzerland) · 2021Review
- Identification of hub genes related to the progression of type 1 diabetes by computational analysis.BMC endocrine disorders · 2021Article
- The Downregulation of ADAM17 Exerts Protective Effects against Cardiac Fibrosis by Regulating Endoplasmic Reticulum Stress and Mitophagy.Oxidative medicine and cellular longevity · 2021Article
- The Role of Epidermal Growth Factor Receptor Family of Receptor Tyrosine Kinases in Mediating Diabetes-Induced Cardiovascular Complications.Frontiers in pharmacology · 2021Review
- Selective deficiency in endothelial PTP1B protects from diabetes and endoplasmic reticulum stress-associated endothelial dysfunction via preventing endothelial cell apoptosis.Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie · 2020Article
- Epidermal Growth Factor Receptor: A Potential Therapeutic Target for Diabetic Kidney Disease.Frontiers in pharmacology · 2020Review
- Cellular Protein Quality Control in Diabetic Cardiomyopathy: From Bench to Bedside.Frontiers in cardiovascular medicine · 2020Review
- Review
- Endoplasmic Reticulum Stress: A Critical Molecular Driver of Endothelial Dysfunction and Cardiovascular Disturbances Associated with Diabetes.International journal of molecular sciences · 2019Review
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7 authors at 1 institution in 1 country.
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Abstract
Epidermal growth factor receptor tyrosine kinase (EGFRtk) and endoplasmic reticulum (ER) stress are important factors in cardiovascular complications. Understanding whether enhanced EGFRtk activity and ER stress induction are involved in cardiac damage, and microvascular dysfunction in type 1 diabetes mellitus is an important question that has remained unanswered. Cardiac fibrosis and microvascular function were determined in C57BL/6J mice injected with streptozotocin only or in combination with EGFRtk inhibitor (AG1478), ER stress inhibitor (Tudca), or insulin for 2 weeks. In diabetic mice, we observed an increase in EGFRtk phosphorylation and ER stress marker expression (CHOP, ATF4, ATF6, and phosphorylated-eIF2α) in heart and mesenteric resistance arteries, which were reduced with AG1478, Tudca, and insulin. Cardiac fibrosis, enhanced collagen type I, and plasminogen activator inhibitor 1 were decreased with AG1478, Tudca, and insulin treatments. The impaired endothelium-dependent relaxation and -independent relaxation responses were also restored after treatments. The inhibition of NO synthesis reduced endothelium-dependent relaxation in control and treated streptozotocin mice, whereas the inhibition of NADPH oxidase improved endothelium-dependent relaxation only in streptozotocin mice. Moreover, in mesenteric resistance arteries, the mRNA levels of Nox2 and Nox4 and the NADPH oxidase activity were augmented in streptozotocin mice and reduced with treatments. This study unveiled novel roles for enhanced EGFRtk phosphorylation and its downstream ER stress in cardiac fibrosis and microvascular endothelial dysfunction in type 1 diabetes mellitus.
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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.