ArticleThe Journal of clinical investigation2004
Determination of the molecular basis of Marfan syndrome: a growth industry.
Article in The Journal of clinical investigation, 2004. 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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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.
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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.
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Who cites it
10 citing papers in PubMed, 41 citations in OpenAlex.
- Aortic asprosin overexpression does not ameliorate disease pathophysiology in a murine model of Marfan syndrome.Scientific reports · 2026Article
- Diagnosis and treatment of cardiovascular disease in patients with heritable connective tissue disorders or heritable thoracic aortic diseases.Cardiovascular intervention and therapeutics · 2024Review
- Novel FBN1 mutations are responsible for cardiovascular manifestations of Marfan syndrome.Molecular biology reports · 2016Article
- Fibrillin-1, induced by Aurora-A but inhibited by BRCA2, promotes ovarian cancer metastasis.Oncotarget · 2015Article
- The ever-expanding conundrum of primary osteoporosis: aetiopathogenesis, diagnosis, and treatment.Italian journal of pediatrics · 2014Review
- Assessment of bone mineral status in children with Marfan syndrome.American journal of medical genetics. Part A · 2012Article
- TGFBR3 variation is not a common cause of Marfan-like syndrome and Loeys-Dietz-like syndrome.Journal of negative results in biomedicine · 2012Article
- Dilatation of the great arteries in an infant with marfan syndrome and ventricular septal defect.Case reports in medicine · 2011Article
- Current themes in molecular pediatrics: molecular medicine and its applications.Italian journal of pediatrics · 2010Review
- The zinc transporter SLC39A13/ZIP13 is required for connective tissue development; its involvement in BMP/TGF-beta signaling pathways.PloS one · 2008Article
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1 author at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Although it has been known for more than a decade that Marfan syndrome - a dominantly inherited connective tissue disorder characterized by tall stature, arachnodactyly, lens subluxation, and a high risk of aortic aneurysm and dissection - results from mutations in the FBN1 gene, which encodes fibrillin-1, the precise mechanism by which the pleiotropic phenotype is produced has been unclear. A report in this issue now proposes that loss of fibrillin-1 protein by any of several mechanisms and the subsequent effect on the pool of TGF-beta may be more relevant in the development of Marfan syndrome than mechanisms previously proposed in a dominant-negative disease model. The model proposed in this issue demonstrates several strategies for clinical intervention.
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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.