Trial reportHypertension (Dallas, Tex. : 1979)2012
Mechanisms of premature vascular aging in children with Hutchinson-Gilford progeria syndrome.
Trial report in Hypertension (Dallas, Tex. : 1979), 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 79 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
79 citing papers in PubMed, 152 citations in OpenAlex.
- Ultrasonic Characteristics of Cardiovascular Changes in Children with Hutchinson-Gilford Progeria Syndrome: A Comparative Study with Normal Children and Aging People.BioMed research international · 2020Trial
- Clinical Trial of the Protein Farnesylation Inhibitors Lonafarnib, Pravastatin, and Zoledronic Acid in Children With Hutchinson-Gilford Progeria Syndrome.Circulation · 2016Trial
- Clinical trial of a farnesyltransferase inhibitor in children with Hutchinson-Gilford progeria syndrome.Proceedings of the National Academy of Sciences of the United States of America · 2012Trial
- Human trilayer engineered blood vessel reveals influence of fibroblasts on disease progression in model of Hutchinson-Gilford progeria.Science advances · 2026Article
- Why and How Are Infants with Hutchinson-Gilford Progeria Syndrome Born Without Severe Manifestations?Medical sciences (Basel, Switzerland) · 2025Review
- Unraveling the mysteries of Hutchinson-Gilford progeria syndrome: a comprehensive review of LMNA gene mutations.Biogerontology · 2025Review
- Targeting CRM1 for Progeria Syndrome Therapy.Aging cell · 2025Article
- Angiopoietin-2: A Therapeutic Target for Vascular Protection in Hutchinson-Gilford Progeria Syndrome.International journal of molecular sciences · 2024Review
- Normal Bone Matrix Mineralization but Altered Growth Plate Morphology in the LmnaAging and disease · 2024Article
- Lipodystrophic Laminopathies: From Dunnigan Disease to Progeroid Syndromes.International journal of molecular sciences · 2024Review
- Article
- Coronary and carotid artery dysfunction and KGeroScience · 2024Article
- Intervention for critical aortic stenosis in Hutchinson-Gilford progeria syndrome.Frontiers in cardiovascular medicine · 2024Article
- Life at the crossroads: the nuclear LINC complex and vascular mechanotransduction.Frontiers in physiology · 2024Review
- Article
- Bone dysplasia in Hutchinson-Gilford progeria syndrome is associated with dysregulated differentiation and function of bone cell populations.Aging cell · 2023Article
- Biomechanical and transcriptional evidence that smooth muscle cell death drives an osteochondrogenic phenotype and severe proximal vascular disease in progeria.Biomechanics and modeling in mechanobiology · 2023Article
- Article
- Building Blood Vessel Chips with Enhanced Physiological Relevance.Advanced materials technologies · 2023Article
- Article
19 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 3 institutions in 1 country.
Funding
Abstract
Hutchinson-Gilford progeria syndrome is a rare, segmental premature aging syndrome of accelerated atherosclerosis and early death from myocardial infarction or stroke. This study sought to establish comprehensive characterization of the fatal vasculopathy in Hutchinson-Gilford progeria syndrome and its relevance to normal aging. We performed cardiovascular assessments at a single clinical site on the largest prospectively studied cohort to date. Carotid-femoral pulse wave velocity was dramatically elevated (mean: 13.00±3.83 m/s). Carotid duplex ultrasound echobrightness, assessed in predefined tissue sites as a measure of arterial wall density, was significantly greater than age- and sex-matched controls in the intima-media (P<0.02), near adventitia (P<0.003), and deep adventitia (P<0.01), as was internal carotid artery mean flow velocity (P<0.0001). Ankle-brachial indices were abnormal in 78% of patients. Effective disease treatments may be heralded by normalizing trends of these noninvasive cardiovascular measures. The data demonstrate that, along with peripheral vascular occlusive disease, accelerated vascular stiffening is an early and pervasive mechanism of vascular disease in Hutchinson-Gilford progeria syndrome. There is considerable overlap with cardiovascular changes of normal aging, which reinforces the view that defining mechanisms of cardiovascular disease in Hutchinson-Gilford progeria syndrome provides a unique opportunity to isolate a subset of factors influencing cardiovascular disease in the general aging population.
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What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.