ArticleJACC. Basic to translational science2024
The Antioxidant/Nitric Oxide-Quenching Agent Cobinamide Prevents Aortic Disease in a Mouse Model of Marfan Syndrome.
Article in JACC. Basic to translational science, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
What it found
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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.
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.
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Who cites it
10 citing papers in PubMed, 5 citations in OpenAlex.
- Gene-Based Rare Variant Burden Analyses Across Biobanks Identify Novel High-Risk Genes for Thoracic Aortic Disease.medRxiv : the preprint server for health sciences · 2026Article
- The aorta in Marfan syndrome: from molecular mechanisms to mechanobiological dysfunction.Cardiovascular research · 2026Review
- Hydrogen Cyanide Generation by Pseudomonas aeruginosa Blunts the Host Innate Immune Response.The Journal of infectious diseases · 2026Article
- Neutralization of reactive oxygen species with cobinamide augments aortic dissections and rupture in BAPN-administered mice.American journal of physiology. Heart and circulatory physiology · 2026Article
- Structural and Signaling Mechanisms of Aortic Wall Failure in Heritable Thoracic Aortic Disease.Cells · 2026Review
- Cobinamide, a Vitamin BToxics · 2026Article
- Meso-fluorinated cobalamins: insights into synthesis and redox properties.Journal of biological inorganic chemistry : JBIC : a publication of the Society of Biological Inorganic Chemistry · 2026Article
- Therapeutic Opportunities of Marfan Syndrome: Current Perspectives.Drug design, development and therapy · 2025Review
- The Antioxidant Vitamin B12 Analogue Cobinamide as a Treatment for Marfan Syndrome.JACC. Basic to translational science · 2024Article
- 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
9 authors at 1 institution in 1 country.
Funding
Abstract
Major pathologic changes in the proximal aorta underlie the life-threatening aortic aneurysms and dissections in Marfan Syndrome; current treatments delay aneurysm development without addressing the primary pathology. Because excess oxidative stress and nitric oxide/protein kinase G signaling likely contribute to the aortopathy, we hypothesized that cobinamide, a strong antioxidant that can attenuate nitric oxide signaling, could be uniquely suited to prevent aortic disease. In a well-characterized mouse model of Marfan Syndrome, cobinamide dramatically reduced elastin breaks, prevented excess collagen deposition and smooth muscle cell apoptosis, and blocked DNA, lipid, and protein oxidation and excess nitric oxide/protein kinase G signaling in the ascending aorta. Consistent with preventing pathologic changes, cobinamide diminished aortic root dilation without affecting blood pressure. Cobinamide exhibited excellent safety and pharmacokinetic profiles indicating it could be a practical treatment. We conclude that cobinamide deserves further study as a disease-modifying treatment of Marfan Syndrome.
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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.