ArticleHuman molecular genetics2020
LRP2 controls sonic hedgehog-dependent differentiation of cardiac progenitor cells during outflow tract formation.
Article in Human molecular genetics, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 21 citations in OpenAlex.
- Biomarkers and immunotherapy in endometrial cancer: mechanisms and clinical applications.Frontiers in immunology · 2025Review
- Cardiomyocyte proliferation and regeneration in congenital heart disease.Pediatric discovery · 2024Article
- Article
- LRP2 contributes to planar cell polarity-dependent coordination of motile cilia function.Cell and tissue research · 2023Article
- Integrated in silico analysis of LRP2 mutations to immunotherapy efficacy in pan-cancer cohort.Discover oncology · 2022Article
- Review
- Quantitative proteomics analysis of human vitreous in rhegmatogenous retinal detachment associated with choroidal detachment by data-independent acquisition mass spectrometry.Molecular and cellular biochemistry · 2022Article
- Cardiac stem cells: Current knowledge and future prospects.World journal of stem cells · 2022Review
- Article
- Endocytic Protein Defects in the Neural Crest Cell Lineage and Its Pathway Are Associated with Congenital Heart Defects.International journal of molecular sciences · 2021Review
- Outflow Tract Formation-Embryonic Origins of Conotruncal Congenital Heart Disease.Journal of cardiovascular development and disease · 2021Review
- Neural tube closure requires the endocytic receptor Lrp2 and its functional interaction with intracellular scaffolds.Development (Cambridge, England) · 2021Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Conotruncal malformations are a major cause of congenital heart defects in newborn infants. Recently, genetic screens in humans and in mouse models have identified mutations in LRP2, a multi-ligand receptor, as a novel cause of a common arterial trunk, a severe form of outflow tract (OFT) defect. Yet, the underlying mechanism why the morphogen receptor LRP2 is essential for OFT development remained unexplained. Studying LRP2-deficient mouse models, we now show that LRP2 is expressed in the cardiac progenitor niche of the anterior second heart field (SHF) that contributes to the elongation of the OFT during separation into aorta and pulmonary trunk. Loss of LRP2 in mutant mice results in the depletion of a pool of sonic hedgehog-dependent progenitor cells in the anterior SHF due to premature differentiation into cardiomyocytes as they migrate into the OFT myocardium. Depletion of this cardiac progenitor cell pool results in aberrant shortening of the OFT, the likely cause of CAT formation in affected mice. Our findings identified the molecular mechanism whereby LRP2 controls the maintenance of progenitor cell fate in the anterior SHF essential for OFT separation, and why receptor dysfunction is a novel cause of conotruncal malformation.
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