ArticleCommunications biology2023
Decreased left heart flow in fetal lambs causes left heart hypoplasia and pro-fibrotic tissue remodeling.
Article in Communications biology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 13 citations in OpenAlex.
- Animal models of hypoplastic left heart syndrome: genetic and anatomical approaches.Pediatric research · 2026Review
- Review
- Preclinical Assessment of Atorvastatin for Treatment of Endocardial Fibroelastosis.JACC. Basic to translational science · 2025Article
- Developmental and Evolutionary Heart Adaptations Through Structure-Function Relationships.Journal of cardiovascular development and disease · 2025Review
- Enhanced myocardial perfusion in late gestation fetal lambs with impaired left ventricular inflow.The Journal of physiology · 2025Article
- In Vivo and In Vitro Approaches to Modeling Hypoplastic Left Heart Syndrome.Current cardiology reports · 2024Review
- Interdependence of placenta and fetal cardiac development.Prenatal diagnosis · 2024Review
- What Is the Hypoplastic Left Heart Syndrome?World journal for pediatric & congenital heart surgery · 2024Article
- Chronic in utero mitral inflow obstruction unloads left ventricular volume in a novel late gestation fetal lamb model.JTCVS open · 2023Article
- Evidence-based treatment strategies for hypoplastic left heart syndrome: The role of EFNA1/EphA.Annals of pediatric cardiologyReview
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Authors and funding
14 authors at 5 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Low blood flow through the fetal left heart is often conjectured as an etiology for hypoplastic left heart syndrome (HLHS). To investigate if a decrease in left heart flow results in growth failure, we generate left ventricular inflow obstruction (LVIO) in mid-gestation fetal lambs by implanting coils in their left atrium using an ultrasound-guided percutaneous technique. Significant LVIO recapitulates important clinical features of HLHS: decreased antegrade aortic valve flow, compensatory retrograde perfusion of the brain and ascending aorta (AAo) from the arterial duct, severe left heart hypoplasia, a non-apex forming LV, and a thickened endocardial layer. The hypoplastic AAo have miRNA-gene pairs annotating to cell proliferation that are inversely differentially expressed by bulk RNA-seq. Single-nucleus RNA-seq of the hypoplastic LV myocardium shows an increase in fibroblasts with a reciprocal decrease in cardiomyocyte nuclei proportions. Fibroblasts, cardiomyocytes and endothelial cells from hypoplastic myocardium have increased expression of extracellular matrix component or fibrosis genes with dysregulated fibroblast growth factor signaling. Hence, a severe sustained ( ~ 1/3 gestation) reduction in fetal left heart flow is sufficient to cause left heart hypoplasia. This is accompanied by changes in cellular composition and gene expression consistent with a pro-fibrotic environment and aberrant induction of mesenchymal programs.
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Registered trials
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