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Reactive oxygen species in cardiovascular disease
Open accessAbstract
Based on the "free radical theory" of disease, researchers have been trying to elucidate the role of oxidative stress from free radicals in cardiovascular disease. Considerable data indicate that reactive oxygen species and oxidative stress are important features of cardiovascular diseases including atherosclerosis, hypertension, and congestive heart failure. However, blanket strategies with antioxidants to ameliorate cardiovascular disease have not generally yielded favorable results. However, our understanding of reactive oxygen species has evolved to the point at which we now realize these species have important roles in physiology as well as pathophysiology. Thus, it is overly simplistic to assume a general antioxidant strategy will yield specific effects on cardiovascular disease. Indeed, there are several sources of reactive oxygen species that are known to be active in the cardiovascular system. This review addresses our understanding of reactive oxygen species sources in cardiovascular disease and both animal and human data defining how reactive oxygen species contribute to physiology and pathology.
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“The expression of NOX4 is upregulated by TGF-β (201, 906).”
From Sources of Vascular Nitric Oxide and Reactive Oxygen Species and Their Regulation (2019) · cites this paper as [906]
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Manu, T. M., Anand, T., Babu, G. R. S., Patil, M. M., & Khanum, F. (2019) · Archives of Physiology and Biochemistry · doi:10.1080/13813455.2019.1683583 · Cited by 11
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Metadata
- Authors
- Sugamura, K., & Keaney
- Affiliations
- University of Massachusetts Chan Medical School (US)
- Corresponding author
- Keaney,, John F.
- Venue
- Free Radical Biology and Medicine
- Publisher
- Elsevier BV
- Published
- 2011-09
- Volume
- 51
- Issue
- 5
- Pages
- 978-992
- ISSN
- 0891-5849 (ISSN-L)
- PMC
- PMC3156326
- OpenAlex
- W2037586146
- Cited by
- 769
- References
- 304
- Citations by year
- 2026: 12 · 2025: 31 · 2024: 40 · 2023: 48 · 2022: 56 · 2021: 48 · 2020: 51 · 2019: 56 · 2018: 58 · 2017: 67 · 2016: 45 · 2015: 69 · 2014: 72 · 2013: 49 · 2012: 58
- FWCI
- 6.50
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Free Radical Biology and Medicine (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- Uehara Memorial Foundation
- Japan Heart Foundation
- National Institutes of Health
- Bayer Yakuhin
- National Heart, Lung, and Blood Institute (HL081587, R01HL098407, P01HL081587, HL098407, HL092122, R01HL092122)
- National Institute of Diabetes and Digestive and Kidney Diseases (DK 32520, P30DK032520)
- Topics
- Health Sciences › Medicine › Physiology (medical) › Nitric Oxide and Endothelin Effects
- Health Sciences › Medicine › Biochemistry (medical) › Antioxidant Activity and Oxidative Stress
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Redox biology and oxidative stress
- Keywords
- reactive oxygen species, oxidative stress, free radicals, cardiovascular disease, atherosclerosis, hypertension, congestive heart failure, antioxidants, antioxidant therapy, redox signaling
- MeSH terms
- Animals, Antioxidants, Cardiovascular Diseases, Clinical Trials as Topic, Heart, Humans, Biomarkers, Reactive Oxygen Species, Oxidative Stress, Molecular Targeted Therapy
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
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