ArticleeLife2016
The Apelin receptor enhances Nodal/TGFβ signaling to ensure proper cardiac development.
Article in eLife, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
23 citing papers in PubMed, 32 citations in OpenAlex.
- Apelin-APLNR pathway across development, inflammation, and vascular remodeling: an endothelial perspective.Experimental & molecular medicine · 2026Review
- International Union of Basic and Clinical Pharmacology. CXXI. Apelin receptor pharmacology in the human cardiovascular system and emerging clinical applications.Pharmacological reviews · 2026Review
- Apelin signaling acts as a molecular switch between endothelial and hematopoietic stem cell fates.EMBO reports · 2026Article
- The small molecule ML233 is a direct inhibitor of tyrosinase function.Communications biology · 2025Article
- The small molecule ML233 is a direct inhibitor of tyrosinase function.bioRxiv : the preprint server for biology · 2025Article
- Single-cell RNA sequencing reveals key regulators and differentiation trajectory of iPSC-derived cardiomyocytes.Scientific reports · 2024Article
- Charting the Path: Navigating Embryonic Development to Potentially Safeguard against Congenital Heart Defects.Journal of personalized medicine · 2023Review
- The Apelinergic System in Pregnancy.International journal of molecular sciences · 2023Review
- Article
- Modeling Human Cardiac Arrhythmias: Insights from Zebrafish.Journal of cardiovascular development and disease · 2022Review
- The SARS-CoV-2 receptor and other key components of the Renin-Angiotensin-Aldosterone System related to COVID-19 are expressed in enterocytes in larval zebrafish.Biology open · 2021Article
- Atrial and Sinoatrial Node Development in the Zebrafish Heart.Journal of cardiovascular development and disease · 2021Review
- HiPS-Endothelial Cells Acquire Cardiac Endothelial Phenotype in Co-culture With hiPS-Cardiomyocytes.Frontiers in cell and developmental biology · 2021Article
- Apelin increases atrial conduction velocity, refractoriness, and prevents inducibility of atrial fibrillation.JCI insight · 2020Article
- Genome-wide CRISPR screen identifies ZIC2 as an essential gene that controls the cell fate of early mesodermal precursors to human heart progenitors.Stem cells (Dayton, Ohio) · 2020Article
- Flow-Induced Transcriptomic Remodeling of Endothelial Cells Derived From Human Induced Pluripotent Stem Cells.Frontiers in physiology · 2020Article
- Decellularized Human Dermal Matrix as a Biological Scaffold for Cardiac Repair and Regeneration.Frontiers in bioengineering and biotechnology · 2020Article
- International Union of Basic and Clinical Pharmacology. CVII. Structure and Pharmacology of the Apelin Receptor with a Recommendation that Elabela/Toddler Is a Second Endogenous Peptide Ligand.Pharmacological reviews · 2019Review
- Aplnra/b Sequentially Regulate Organ Left-Right Patterning via Distinct Mechanisms.International journal of biological sciences · 2019Article
- Apelinergic System Structure and Function.Comprehensive Physiology · 2017Review
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
Abstract
The Apelin receptor (Aplnr) is essential for heart development, controlling the early migration of cardiac progenitors. Here we demonstrate that in zebrafish Aplnr modulates Nodal/TGFβ signaling, a key pathway essential for mesendoderm induction and migration. Loss of Aplnr function leads to a reduction in Nodal target gene expression whereas activation of Aplnr by a non-peptide agonist increases the expression of these same targets. Furthermore, loss of Aplnr results in a delay in the expression of the cardiogenic transcription factors mespaa/ab. Elevating Nodal levels in aplnra/b morphant and double mutant embryos is sufficient to rescue cardiac differentiation defects. We demonstrate that loss of Aplnr attenuates the activity of a point source of Nodal ligands Squint and Cyclops in a non-cell autonomous manner. Our results favour a model in which Aplnr is required to fine-tune Nodal output, acting as a specific rheostat for the Nodal/TGFβ pathway during the earliest stages of cardiogenesis.
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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.