ArticleeLife2022
Apelin signaling dependent endocardial protrusions promote cardiac trabeculation in zebrafish.
Article in eLife, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
What it found
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Who cites it
9 citing papers in PubMed, 19 citations in OpenAlex.
- Adgrg6/Gpr126 is required for compact wall integrity and establishing trabecular identity during cardiac trabeculation.Nature communications · 2026Article
- Apelin signaling acts as a molecular switch between endothelial and hematopoietic stem cell fates.EMBO reports · 2026Article
- Construction of a Zebrafish Model of Cardiac Hypertrophy Caused by ATIC Gene Deletion and Preliminary Exploration of Aerobic Exercise Improvement.International journal of molecular sciences · 2025Article
- The Mechanics of Building Functional Organs.Cold Spring Harbor perspectives in biology · 2025Review
- Distinct mechanisms regulate ventricular and atrial chamber wall formation.Nature communications · 2024Article
- Mechanical forces remodel the cardiac extracellular matrix during zebrafish development.Development (Cambridge, England) · 2024Article
- A β-catenin chromobody-based probe highlights endothelial maturation during vascular morphogenesis in vivo.Development (Cambridge, England) · 2024Article
- The MEK-ERK signaling pathway promotes maintenance of cardiac chamber identity.Development (Cambridge, England) · 2024Article
- The developing epicardium regulates cardiac chamber morphogenesis by promoting cardiomyocyte growth.Disease models & mechanisms · 2023Article
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
During cardiac development, endocardial cells (EdCs) produce growth factors to promote myocardial morphogenesis and growth. In particular, EdCs produce neuregulin which is required for ventricular cardiomyocytes (CMs) to seed the multicellular ridges known as trabeculae. Defects in neuregulin signaling, or in endocardial sprouting toward CMs, cause hypotrabeculation. However, the mechanisms underlying endocardial sprouting remain largely unknown. Here, we first show by live imaging in zebrafish embryos that EdCs interact with CMs via dynamic membrane protrusions. After touching CMs, these protrusions remain in close contact with their target despite the vigorous cardiac contractions. Loss of the CM-derived peptide Apelin, or of the Apelin receptor, which is expressed in EdCs, leads to reduced endocardial sprouting and hypotrabeculation. Mechanistically, neuregulin signaling requires endocardial protrusions to induce extracellular signal-regulated kinase (Erk) activity in CMs and trigger their delamination. Altogether, these data show that Apelin signaling-dependent endocardial protrusions modulate CM behavior during trabeculation.
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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.