ArticleCommunications biology2022
Alteration in tyrosine phosphorylation of cardiac proteome and EGFR pathway contribute to hypertrophic cardiomyopathy.
Article in Communications biology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 14 citations in OpenAlex.
- Identifying ROCK2 as an intervention target for bilirubin encephalopathy.Fundamental research · 2026Article
- Signaling pathway alterations in hearts of a porcine model harboring a β-myosin heavy chain (MYH7-R403Q) gene variant.Journal of molecular and cellular cardiology plus · 2025Article
- The Protective Mechanism of Moderate Intensity Continuous Training on TMAO-Induced Myocardial Injury Based on NMR Metabolomics.International journal of molecular sciences · 2025Article
- Exploration of calcium and amino acids for children with primary cardiomyopathies based on genetic characteristics.Frontiers in pediatrics · 2025Article
- Integrative proteomic and metabolomic elucidation of cardiomyopathy with in vivo and in vitro models and clinical samples.Molecular therapy : the journal of the American Society of Gene Therapy · 2024Review
- Machine learning and experimental validation of novel biomarkers for hypertrophic cardiomyopathy and cancers.Journal of cellular and molecular medicine · 2024Article
- Proteomics of the heart.Physiological reviews · 2024Review
- Mechanisms Underlying the Therapeutic Effects of Nicotinamide Mononucleotide in Treating High-fat Diet-induced Hypertrophic Cardiomyopathy based on GEO Datasets, Network Pharmacology, and Molecular Docking.Current pharmaceutical design · 2024Article
- Cardiometabolic Modulation by Semaglutide Contributes to Cardioprotection in Rats with Myocardial Infarction.Drug design, development and therapy · 2024Article
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Authors and funding
16 authors at 4 institutions in 3 countries.
Funding
Abstract
Alterations of serine/threonine phosphorylation of the cardiac proteome are a hallmark of heart failure. However, the contribution of tyrosine phosphorylation (pTyr) to the pathogenesis of cardiac hypertrophy remains unclear. We use global mapping to discover and quantify site-specific pTyr in two cardiac hypertrophic mouse models, i.e., cardiac overexpression of ErbB2 (TgErbB2) and α myosin heavy chain R403Q (R403Q-αMyHC Tg), compared to control hearts. From this, there are significant phosphoproteomic alterations in TgErbB2 mice in right ventricular cardiomyopathy, hypertrophic cardiomyopathy (HCM), and dilated cardiomyopathy (DCM) pathways. On the other hand, R403Q-αMyHC Tg mice indicated that the EGFR1 pathway is central for cardiac hypertrophy, along with angiopoietin, ErbB, growth hormone, and chemokine signaling pathways activation. Surprisingly, most myofilament proteins have downregulation of pTyr rather than upregulation. Kinase-substrate enrichment analysis (KSEA) shows a marked downregulation of MAPK pathway activity downstream of k-Ras in TgErbB2 mice and activation of EGFR, focal adhesion, PDGFR, and actin cytoskeleton pathways. In vivo ErbB2 inhibition by AG-825 decreases cardiomyocyte disarray. Serine/threonine and tyrosine phosphoproteome confirm the above-described pathways and the effectiveness of AG-825 Treatment. Thus, altered pTyr may play a regulatory role in cardiac hypertrophic models.
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