ArticleBMC molecular and cell biology2019
ERK1/2 communicates GPCR and EGFR signaling pathways to promote CTGF-mediated hypertrophic cardiomyopathy upon Ang-II stimulation.
Article in BMC molecular and cell biology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 9 citations in OpenAlex.
- The Role of Signalling Pathways in Myocardial Fibrosis in Hypertrophic Cardiomyopathy.Reviews in cardiovascular medicine · 2025Review
- Oxidative Stress: A Culprit in the Progression of Diabetic Kidney Disease.Antioxidants (Basel, Switzerland) · 2024Review
- Advances in oxidative stress in pathogenesis of diabetic kidney disease and efficacy of TCM intervention.Renal failure · 2023Review
- 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
- Identification of key genes for hypertrophic cardiomyopathy using integrated network analysis of differential lncRNA and gene expression.Frontiers in cardiovascular medicine · 2022Article
- Epigenetic role of N6-methyladenosine (m6A) RNA methylation in the cardiovascular system.Journal of Zhejiang University. Science. B · 2020Review
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Authors and funding
7 authors at 1 institution in 1 country.
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Abstract
backgroundHypertrophic cardiomyopathy occurs along with pathological phenomena such as cardiac hypertrophy, myocardial fibrosis and cardiomyocyte activity. However, few of the specific molecular mechanisms underlying this pathological condition have been mentioned.
methodsAll target proteins and markers expression in the study was verified by PCR and western bloting. H9c2 cell morphology and behavior were analyzed using immunofluorescent and proliferation assays, respectively. And, the CTGF protein secreted in cell culture medium was detected by ELISA.
resultsWe found that high expression of CTGF and low expression of EGFR were regulated by ERK1/2 signaling pathway during the cardiac hypertrophy induced by Ang-II stimulation. CTGF interacted with EGFR, and the interaction is reduced with the stimulation of Ang-II. ERK1/2 serves as the center of signal control during the cardiac hypertrophy.
conclusionThe ERK1/2 cooperates with GPCR and EGFR signaling, and promotes the occurrence and development of cardiac hypertrophy by regulating the expression and binding states of CTGF and EGFR. The study revealed a regulation model based on ERK1/2, suggesting that ERK1/2 signaling pathway may be an important control link for mitigation of hypertrophic cardiomyopathy treatment.
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