ArticleCellular signalling2017
Endothelin-1 promotes hypertrophic remodelling of cardiac myocytes by activating sustained signalling and transcription downstream of endothelin type A receptors.
Article in Cellular signalling, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.
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Who cites it
38 citing papers in PubMed, 83 citations in OpenAlex.
- Macitentan attenuates cardiovascular remodelling in infant rats with chronic lung disease.Journal of translational medicine · 2022Trial
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- Human iPSC-derived cardiac-specific extracellular matrix scaffolds for cardiomyocyte maturation and post-myocardial infarction repair.Bioactive materials · 2026Article
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- BubR1 Controls Heart Development by Promoting Expression of Cardiogenesis Regulators.Journal of the American Heart Association · 2025Article
- Cardiovascular effects and safety of classic psychedelics.Nature cardiovascular research · 2025Review
- Gut microbiota and atrial cardiomyopathy.Frontiers in cardiovascular medicine · 2025Review
- The Complex Role of Matrix Metalloproteinase-2 (MMP-2) in Health and Disease.International journal of molecular sciences · 2024Review
- In Vitro Models of Cardiovascular Disease: Embryoid Bodies, Organoids and Everything in Between.Biomedicines · 2024Review
- Catecholamine treatment induces reversible heart injury and cardiomyocyte gene expression.Intensive care medicine experimental · 2024Article
- Evaluation of Tyrosine Kinase Inhibitors Loaded Injectable Hydrogels for Improving Connexin43 Gap Junction Intercellular Communication.ACS applied materials & interfaces · 2024Article
- Epicardioid single-cell genomics uncovers principles of human epicardium biology in heart development and disease.Nature biotechnology · 2023Article
- Endothelin Receptor Blocker Reverses Breast Cancer-Induced Cardiac Remodeling.JACC. CardioOncology · 2023Article
- The secretome as a biomarker and functional agent in heart failure.The journal of cardiovascular aging · 2023Article
- Impact of Intratracheal Administration of Polyethylene Glycol-Coated Silver Nanoparticles on the Heart of Normotensive and Hypertensive Mice.International journal of molecular sciences · 2023Article
- Morphological and Functional Remodeling of the Ischemic Heart Correlates with Homocysteine Levels.Journal of cardiovascular development and disease · 2023Article
- Endothelin-1 Induces Cell Proliferation and Myofibroblast Differentiation through the ETInternational journal of molecular sciences · 2023Article
- Biocompatibility of Subperiosteal Dental Implants: Effects of Differently Treated Titanium Surfaces on the Expression of ECM-Related Genes in Gingival Fibroblasts.Journal of functional biomaterials · 2023Article
- NLRP3 activation contributes to endothelin-1-induced erectile dysfunction.Journal of cellular and molecular medicine · 2023Article
- Endothelial cell dysfunction in cardiac disease: driver or consequence?Frontiers in cell and developmental biology · 2023Review
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
Abstract
G-protein coupled receptor (GPCR) mediated activation of the MAPK signalling cascade is a key pathway in the induction of hypertrophic remodelling of the heart - a response to pathological cues including hypertension and myocardial infarction. While levels of pro-hypertrophic hormone agonists of GPCRs increase during periods of greater workload to enhance cardiac output, hypertrophy does not necessarily result. Here we investigated the relationship between the duration of exposure to the pro-hypertrophic GPCR agonist endothelin-1 (ET-1) and the induction of hypertrophic remodelling in neonatal rat ventricular myocytes (NRVM) and in the adult rat heart in vivo. Notably, a 15min pulse of ET-1 was sufficient to induce markers of hypertrophy that were present when measured at 24h in vivo and 48h in vitro. The persistence of ET-1 action was insensitive to ET type A receptor (ET
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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.