ArticleArteriosclerosis, thrombosis, and vascular biology2025
Chemokine (C-C Motif) Ligand 2 Expressing Adventitial Fibroblast Expansion During Loeys-Dietz Syndrome Aortic Aneurysm Formation.
Article in Arteriosclerosis, thrombosis, and vascular biology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed.
- Genetic and molecular mechanisms of hereditary thoracic aortic aneurysm and dissection (Review).Molecular medicine reports · 2026Review
- Preclinical modeling of Loeys-Dietz syndrome: insights into mechanisms and therapy.Orphanet journal of rare diseases · 2026Review
- Mechanotransduction in Marfan Syndrome and Related Aortic Disorders: Insights from Transcriptomic Analyses.Genes · 2026Review
- Mechanistic Insight into PVAT Browning as a Protective Factor in Thoracic Aortic Aneurysm.Current atherosclerosis reports · 2026Review
- Vascular adventitial cells and vascular remodeling: when a harp of thousand strings does not keep in tune so long.Frontiers in physiology · 2026Review
- VSMCs and the immune microenvironment: a multidimensional regulatory network driving vascular injury and repair.Frontiers in immunology · 2026Review
- Loeys-Dietz syndrome subtypes exhibit distinct clinical behavior and aortic cellular transcriptomic profiles.JTCVS open · 2025Article
- Transforming growth factor-beta (TGF-β) in the pathogenesis of hereditary thoracic aneurysm disorders.Cardiovascular pathology : the official journal of the Society for Cardiovascular PathologyReview
Corrections and comments
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Authors and funding
15 authors.
Funding
Abstract
backgroundLoeys-Dietz syndrome (LDS), caused by mutations in the TGF-β (transforming growth factor-β) signaling cascade, leads to aggressive thoracic aneurysms. While vascular smooth muscle cell (SMC) phenotype modulation has been implicated in thoracic aneurysm formation, we sought to characterize the role of cell state transitions in LDS aneurysm pathogenesis.
methodsWe performed single-cell transcriptomic characterization of aortic root/ascending aorta from a murine LDS model (
resultsInstead of SMC phenotypic modulation seen in Marfan syndrome, transcriptomic alterations observed in LDS are most prominent in the adventitial fibroblast in the
conclusionsDespite phenotypic similarities in aneurysm formation, the dominant cellular and molecular mechanism of Marfan syndrome and LDS aneurysms are distinct. LDS mouse and human adventitial fibroblasts transcriptomically modulate into a proinflammatory state. Adventitial fibroblasts, in addition to SMCs, are another important pathological cell population during LDS aneurysm formation to consider for targeted therapy to potentially impede LDS aneurysm formation.
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