In one paragraphArticle in American journal of physiology. Heart and circulatory physiology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
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.
2 · The registryThe 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.
3 · Its place in the literatureWho cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
4 · The recordCorrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
5 · Who and what moneyAuthors and funding
9 authors.
Alexis RichardDivision of Medical Genetics, Department of Internal Medicine, McGovern Medical School, The University of Texas Health Science Center at Houston, Houston, Texas, United States.ORCID 0009-0000-0461-3160 Zhen ZhouDivision of Medical Genetics, Department of Internal Medicine, McGovern Medical School, The University of Texas Health Science Center at Houston, Houston, Texas, United States.ORCID 0000-0002-7880-5998 Jose Emiliano Esparza PineloDivision of Medical Genetics, Department of Internal Medicine, McGovern Medical School, The University of Texas Health Science Center at Houston, Houston, Texas, United States.
Callie S KwartlerDivision of Medical Genetics, Department of Internal Medicine, McGovern Medical School, The University of Texas Health Science Center at Houston, Houston, Texas, United States.ORCID 0000-0002-3722-9939 Hema KalyanaramanDepartment of Medicine, University of California San Diego, La Jolla, California, United States.ORCID 0000-0003-4870-937X Gerry R BossDepartment of Medicine, University of California San Diego, La Jolla, California, United States.
Hong S LuDepartment of Physiology, Saha Cardiovascular Research Center, Saha Aortic Center, University of Kentucky, Lexington, Kentucky, United States.ORCID 0000-0002-0577-2558 Alan DaughertyDepartment of Physiology, Saha Cardiovascular Research Center, Saha Aortic Center, University of Kentucky, Lexington, Kentucky, United States.ORCID 0000-0003-2093-3775 Dianna M MilewiczDivision of Medical Genetics, Department of Internal Medicine, McGovern Medical School, The University of Texas Health Science Center at Houston, Houston, Texas, United States.ORCID 0000-0002-7806-0068 Funding
Genetic Predisposition To Thoracic Aortic Aneurysms/DissectionsR01HL109942 · NHLBI · UNIVERSITY OF TEXAS HLTH SCI CTR HOUSTON · PI MILEWICZ, DIANNA M · 2012 to 2023
$7.5MTGFb-Dependent Cell-Matrix Interactions in Thoracic AortopathyP01HL169168 · NHLBI · YALE UNIVERSITY · PI Stefania Nicoli · 2025 to 2026
$7.4MNovel genetic Insight into the molecular pathogenesis of atherosclerosisR01HL146583 · NHLBI · UNIVERSITY OF TEXAS HLTH SCI CTR HOUSTON · PI MILEWICZ, DIANNA M · 2019 to 2022
$2.6MFondation Leducq (Leducq Foundation) 22CVD03HHS | NIH | National Heart, Lung, and Blood Institute (NHLBI) 5R01HL146583HHS | NIH | National Heart, Lung, and Blood Institute (NHLBI) P01HL169168HHS | NIH | National Heart, Lung, and Blood Institute (NHLBI) R01HL109942NHLBI NIH HHS P01 HL169168NHLBI NIH HHS R01 HL109942NHLBI NIH HHS R01 HL146583
6 · The paper itselfAbstract
Thoracic aortic aneurysms involving the root and ascending aorta progressively enlarge and can lead to life-threatening acute aortic dissections, collectively termed thoracic aortic disease (TAD). Oxidative stress due to an excess of reactive oxygen species (ROS) has been implicated in TAD pathogenesis by promoting vascular inflammation, extracellular matrix degradation, and smooth muscle cell apoptosis. Cobinamide (Cbi), a potent antioxidant and vitamin B12 analog, has been reported to slow aortic aneurysm growth in TAD mouse models. We evaluated its efficacy in mice administered β-aminopropionitrile (BAPN) to induce TAD, a model in which aneurysms progress to dissections. C57BL/6J mice of both sexes were administered either BAPN alone or BAPN plus Cbi in drinking water from
Indexed as
AminopropionitrileAntioxidantsAorta, ThoracicAortic Aneurysm, ThoracicAortic DissectionAortic RuptureOxidative StressReactive Oxygen SpeciesAnimalsCobamidesDisease Models, AnimalDissection, Thoracic AortaFemaleMaleMiceMice, Inbred C57BLAminopropionitrileAntioxidantsCobamidescobinamideReactive Oxygen Speciesantioxidant therapyaortic dissectionoxidative stressreactive oxygen speciesthoracic aortic disease
Identifiers
PMID42363828
PMCPMC13653532
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