ArticleScientific reports2016
Prokineticin receptor-1 signaling promotes Epicardial to Mesenchymal Transition during heart development.
Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 28 citations in OpenAlex.
- Psycho-cardiovascular interaction network in cardiovascular health and disease: signaling pathways and molecular mechanisms.Precision clinical medicine · 2026Review
- Epicardial cell activation as a paradigm shift in cardiac repair and regeneration.Stem cells translational medicine · 2026Review
- Epicardium-myocardium crosstalk orchestrates heart development.Frontiers in cell and developmental biology · 2025Review
- Therapeutic Potential of Targeting Prokineticin Receptors in Diseases.Pharmacological reviews · 2023Review
- Recapturing embryonic potential in the adult epicardium: Prospects for cardiac repair.Stem cells translational medicine · 2021Review
- Trehalose Ameliorates Diabetic Cardiomyopathy: Role of the PK2/PKR Pathway.Oxidative medicine and cellular longevity · 2021Article
- Updates on Anticancer Therapy-Mediated Vascular Toxicity and New Horizons in Therapeutic Strategies.Frontiers in cardiovascular medicine · 2021Review
- Role of carotenoids and retinoids during heart development.Biochimica et biophysica acta. Molecular and cell biology of lipids · 2020Review
- Prokineticin signaling in heart-brain developmental axis: Therapeutic options for heart and brain injuries.Pharmacological research · 2020Review
- Prokineticin 2 (PK2) Rescues Cardiomyocytes from High Glucose/High Palmitic Acid-Induced Damage by Regulating the AKT/GSK3Oxidative medicine and cellular longevity · 2020Article
- Metformin Ameliorates Diabetic Cardiomyopathy by Activating the PK2/PKR Pathway.Frontiers in physiology · 2020Article
- Prokineticin Receptor-1 Signaling Inhibits Dose- and Time-Dependent Anthracycline-Induced Cardiovascular Toxicity Via Myocardial and Vascular Protection.JACC. CardioOncology · 2019Article
- Targeting GPCRs Against Cardiotoxicity Induced by Anticancer Treatments.Frontiers in cardiovascular medicine · 2019Review
- Prokineticin receptor-1-dependent paracrine and autocrine pathways control cardiac tcf21Scientific reports · 2017Article
- Exploration of haplotype research consortium imputation for genome-wide association studies in 20,032 Generation Scotland participants.Genome medicine · 2017Article
- Prokineticin Is a New Linker between Obesity and Cardiovascular Diseases.Frontiers in cardiovascular medicine · 2017Review
Corrections and comments
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Authors and funding
8 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The epicardium plays an essential role in coronary artery formation and myocardial development. However, signals controlling the developing epicardium and epicardial-mesenchymal transition (EMT) in the normal and diseased adult heart are studied less rigorously. Here we investigated the role of angiogenic hormone, prokineticin-2 and its receptor PKR1 in the epicardium of developing and adult heart. Genetic ablation of PKR1 in epicardium leads to partial embryonic and postnatal lethality with abnormal heart development. Cardiac developmental defects are manifested in the adult stage as ischemic cardiomyopathy with systolic dysfunction. We discovered that PKR1 regulates epicardial-mesenchymal transition (EMT) for epicardial-derived progenitor cell (EPDC), formation. This event affects at least three consequential steps during heart development: (i) EPDC and cardiomyocyte proliferation involved in thickening of an outer compact ventricular chamber wall, (ii) rhythmicity, (iii) formation of coronary circulation. In isolated embryonic EPDCs, overexpression or activation of PKR1 alters cell morphology and EMT markers via activating Akt signaling. Lack of PKR1 signal in epicardium leads to defective heart development and underlies the origin of congenital heart disease in adult mice. Our mice provide genetic models for congenital dysfunction of the heart and should facilitate studies of both pathogenesis and therapy of cardiac disorders in humans.
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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.