ArticleCirculation2022
Second Heart Field-Derived Cells Contribute to Angiotensin II-Mediated Ascending Aortopathies.
Article in Circulation, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
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Who cites it
36 citing papers in PubMed, 55 citations in OpenAlex.
- Article
- Angiotensin II Induces Abdominal Aortic Branch Aneurysms inArteriosclerosis, thrombosis, and vascular biology · 2026Article
- Preclinical modeling of Loeys-Dietz syndrome: insights into mechanisms and therapy.Orphanet journal of rare diseases · 2026Review
- Structural and Signaling Mechanisms of Aortic Wall Failure in Heritable Thoracic Aortic Disease.Cells · 2026Review
- Sparcl1 mitigates abdominal aortic aneurysm through inhibiting lymphangiogenesis-mediated TLS formation.Nature immunology · 2026Article
- Animal Models of Aortic Aneurysm and Dissection: A Comparative Guide for Mechanism, Therapeutic Testing, and Translational Readouts.Biomedicines · 2026Review
- Article
- Galectin-3 is dispensable for thoracic aortic aneurysmal formation and rupture in mice.JVS-vascular science · 2026Article
- Metformin does not attenuate angiotensin II-induced aortic aneurysms in low-density lipoprotein receptor deficient mice.Scientific reports · 2025Article
- A cell and transcriptome atlas of human arterial vasculature.Cell genomics · 2025Article
- Cardiac Hemorrhage Precedes Hypertension-induced Fibrosis in Plasminogen Activator Inhibitor-1 Deficient Mice.bioRxiv : the preprint server for biology · 2025Article
- Endothelium- and Fibroblast-Derived C-Type Natriuretic Peptide Prevents the Development and Progression of Aortic Aneurysm.Arteriosclerosis, thrombosis, and vascular biology · 2025Article
- Smooth muscle cells and fibroblasts in the ascending aorta exhibit minor differences between embryonic origins in angiotensin II-driven transcriptional alterations.Scientific reports · 2025Article
- Origins of Aortic Coarctation: A Vascular Smooth Muscle Compartment Boundary Model.Journal of developmental biology · 2025Article
- Mitochondrial NADNature cardiovascular research · 2025Article
- Single-Cell Transcriptomics Identifies Selective Lineage-Specific Regulation of Genes in Aortic Smooth Muscle Cells in Mice.Arteriosclerosis, thrombosis, and vascular biology · 2025Article
- Correcting mitochondrial loss mitigates NOTCH1-related aortopathy in mice.Nature cardiovascular research · 2025Article
- Unraveling Elastic Fiber-Derived Signaling in Arterial Aging and Related Arterial Diseases.Biomolecules · 2025Review
- Site-specific genetic and functional signatures of aortic endothelial cells at aneurysm predilection sites in healthy and AngII ApoEAngiogenesis · 2024Article
- β-Aminopropionitrile Induces Distinct Pathologies in the Ascending and Descending Thoracic Aortic Regions of Mice.Arteriosclerosis, thrombosis, and vascular biology · 2024Article
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Authors and funding
19 authors at 4 institutions in 2 countries.
Funding
Abstract
backgroundThe ascending aorta is a common location for aneurysm and dissection. This aortic region is populated by a mosaic of medial and adventitial cells that are embryonically derived from either the second heart field (SHF) or the cardiac neural crest. SHF-derived cells populate areas that coincide with the spatial specificity of thoracic aortopathies. The purpose of this study was to determine whether and how SHF-derived cells contribute to ascending aortopathies.
methodsAscending aortic pathologies were examined in patients with sporadic thoracic aortopathies and angiotensin II (AngII)-infused mice. Ascending aortas without overt pathology from AngII-infused mice were subjected to mass spectrometry-assisted proteomics and molecular features of SHF-derived cells were determined by single-cell transcriptomic analyses. Genetic deletion of either
resultsPathologies in human ascending aortic aneurysmal tissues were predominant in outer medial layers and adventitia. This gradient was mimicked in mouse aortas after AngII infusion that was coincident with the distribution of SHF-derived cells. Proteomics indicated that brief AngII infusion before overt pathology occurred evoked downregulation of smooth muscle cell proteins and differential expression of extracellular matrix proteins, including several LRP1 ligands. LRP1 deletion in SHF-derived cells augmented AngII-induced ascending aortic aneurysm and rupture. Single-cell transcriptomic analysis revealed that brief AngII infusion decreased
conclusionsSHF-derived cells exert a critical role in maintaining vascular integrity through LRP1 and transforming growth factor-β signaling associated with increases of aortic PAI1.
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