ReviewCurrent atherosclerosis reports2006
Genetic markers of oxidative stress and coronary atherosclerosis.
Review in Current atherosclerosis reports, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers, 1 of them a synthesis that pooled it.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
4 citing papers in PubMed, 1 synthesis or guideline pooled it, 16 citations in OpenAlex.
- Pooled it
- Patients with Coronary Artery Disease Have Lower Levels of Antibody to Heat-Stressed Fibroblast Derived Proteins, versus Normal Subjects.Cardiovascular therapeutics · 2021Article
- Association of LT-alpha Ala252Gly gene polymorphism and the genetic predisposition of coronary heart disease in Chinese.Molecular biology reports · 2010Article
- Relationship between hemorheology and Glu(298)Asp polymorphism of endothelial nitric oxide synthase gene in patients with coronary artery disease.Molecular biology reports · 2010Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Atherosclerosis, the primary cause of coronary artery disease (CAD), is a multifactorial disease, the molecular etiology of which involves interaction of many genes and environmental factors. Reactive oxygen species are integral to many cellular and biomolecular processes that are active in the transition of incipient fatty streaks into acute coronary syndromes. Animal models of atherosclerosis and correlative data from human studies support the oxidative stress hypothesis of atherosclerosis. However, the association of genetic polymorphisms that underlie enhanced oxidative stress with CAD is controversial. In this review, we discuss polymorphisms in genes that are main sources of reactive oxygen species generation (NADH oxidase, endothelial nitric oxide synthase, and myeloperoxidase) in mitochondria and the antioxidant enzymes paraoxonase, glutathione reductase, and heme oxygenase. The contribution of defined genetic variants involved in oxidative homeostasis to human atherosclerosis susceptibility is modest because regulation of oxidative stress is multifactorial. However, the contribution of genetic haplotypes in concert with environmental factors is likely significant. A more rigorous characterization of genetic and oxidative phenotypes together with characterization of novel gene polymorphisms may help in early therapeutic intervention for CAD.
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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.