ArticleNature cardiovascular research2024
Integrative gene regulatory network analysis discloses key driver genes of fibromuscular dysplasia.
Article in Nature cardiovascular research, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed.
- Prevalence of aortic findings among patients with multifocal fibromuscular dysplasia (FMD) seen at a specialised referral centre.Open heart · 2026Article
- Haemodynamic and biomechanical biomarker analysis of carotid fibromuscular dysplasia via fluid-structure interaction.Biomechanics and modeling in mechanobiology · 2026Article
- Characteristics of patients with extracranial cervical artery dissections involving more than a single vessels: A subgroup analysis of STOP-CAD.European stroke journal · 2026Article
- Cerebrovascular fibromuscular dysplasia.Therapeutic advances in neurological disorders · 2026Review
- The Australian-New Zealand SCAD observational cohort study: major adverse cardiovascular events are associated with ticagrelor combined with aspirin, FMD, and history of stroke.European heart journal · 2025Article
- Case Report: Decoding genetic risks of vascular parkinsonism: a case series.Frontiers in genetics · 2025Article
- Endothelial cells as paracrine mediators of long COVID.Nature cardiovascular research · 2024Article
Corrections and comments
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Authors and funding
33 authors.
Funding
Abstract
Fibromuscular dysplasia (FMD) is a poorly understood disease affecting 3-5% of adult females. The pathobiology of FMD involves arterial lesions of stenosis, dissection, tortuosity, dilation and aneurysm, which can lead to hypertension, stroke, myocardial infarction and even death. Currently, there are no animal models for FMD and few insights as to its pathobiology. In this study, by integrating DNA genotype and RNA sequence data from primary fibroblasts of 83 patients with FMD and 71 matched healthy controls, we inferred 18 gene regulatory co-expression networks, four of which were found to act together as an FMD-associated supernetwork in the arterial wall. After in vivo perturbation of this co-expression supernetwork by selective knockout of a top network key driver, mice developed arterial dilation, a hallmark of FMD. Molecular studies indicated that this supernetwork governs multiple aspects of vascular cell physiology and functionality, including collagen/matrix production. These studies illuminate the complex causal mechanisms of FMD and suggest a potential therapeutic avenue for this challenging disease.
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