ArticleProceedings of the National Academy of Sciences of the United States of America2005
Cardiomyocyte hypertrophy and degradation of connexin43 through spatially restricted autocrine/paracrine heparin-binding EGF.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
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Who cites it
32 citing papers in PubMed, 61 citations in OpenAlex.
- The network response to Egf is tissue-specific.iScience · 2025Article
- Neuropeptide signaling network of Caenorhabditis elegans: from structure to behavior.Genetics · 2024Review
- DNMT3A clonal hematopoiesis-driver mutations induce cardiac fibrosis by paracrine activation of fibroblasts.Nature communications · 2024Article
- The neuropeptidergic connectome of C. elegans.Neuron · 2023Article
- Autocrine Signaling in Cardiac Remodeling: A Rich Source of Therapeutic Targets.Journal of the American Heart Association · 2021Review
- ADAM12 controls a hypertrophic response in the heart through the distinct descending pathways.American journal of physiology. Heart and circulatory physiology · 2020Article
- How doesWorld journal of gastroenterology · 2019Review
- EGFR activation triggers cellular hypertrophy and lysosomal disease in NAGLU-depleted cardiomyoblasts, mimicking the hallmarks of mucopolysaccharidosis IIIB.Cell death & disease · 2018Article
- 11β-HSD1 inhibition ameliorates diabetes-induced cardiomyocyte hypertrophy and cardiac fibrosis through modulation of EGFR activity.Oncotarget · 2017Article
- Exosomes from pediatric dilated cardiomyopathy patients modulate a pathological response in cardiomyocytes.American journal of physiology. Heart and circulatory physiology · 2017Article
- Heparin Promotes Cardiac Differentiation of Human Pluripotent Stem Cells in Chemically Defined Albumin-Free Medium, Enabling Consistent Manufacture of Cardiomyocytes.Stem cells translational medicine · 2017Article
- Article
- Targeting autocrine HB-EGF signaling with specific ADAM12 inhibition using recombinant ADAM12 prodomain.Scientific reports · 2015Article
- Aliskiren-attenuated myocardium apoptosis via regulation of autophagy and connexin-43 in aged spontaneously hypertensive rats.Journal of cellular and molecular medicine · 2014Article
- Regional mapping of myocardial hibernation phenotype in idiopathic end-stage dilated cardiomyopathy.Journal of cellular and molecular medicine · 2014Article
- Dual modes of motility at the leading edge of migrating epithelial cell sheets.Proceedings of the National Academy of Sciences of the United States of America · 2012Article
- Mechanisms of ventricular arrhythmias: a dynamical systems-based perspective.American journal of physiology. Heart and circulatory physiology · 2012Review
- The heparin-binding domain of HB-EGF mediates localization to sites of cell-cell contact and prevents HB-EGF proteolytic release.Journal of cell science · 2010Article
- An EGFR autocrine loop encodes a slow-reacting but dominant mode of mechanotransduction in a polarized epithelium.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2010Article
- Electrical remodeling in the failing heart.Current opinion in cardiology · 2010Review
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Growth factor signaling can affect tissue remodeling through autocrine/paracrine mechanisms. Recent evidence indicates that EGF receptor transactivation by heparin-binding EGF (HB-EGF) contributes to hypertrophic signaling in cardiomyocytes. Here, we show that HB-EGF operates in a spatially restricted circuit in the extracellular space within the myocardium, revealing the critical nature of the local microenvironment in intercellular signaling. This highly localized microenvironment of HB-EGF signaling was demonstrated with 3D morphology, consistent with predictions from a computational model of EGF signaling. HB-EGF secretion by a given cardiomyocyte in mouse left ventricles led to cellular hypertrophy and reduced expression of connexin43 in the overexpressing cell and in immediately adjacent cells but not in cells farther away. Thus, HB-EGF acts as an autocrine and local paracrine cardiac growth factor that leads to loss of gap junction proteins within a spatially confined microenvironment. These findings demonstrate how cells can coordinate remodeling with their immediate neighboring cells with highly localized extracellular EGF signaling.
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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.