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Mitochondrial dysfunction in cardiovascular disease
Abstract
Whereas the pathogenesis of atherosclerosis has been intensively studied and described, the underlying events that initiate cardiovascular disease are not yet fully understood. A substantial number of studies suggest that altered levels of oxidative and nitrosoxidative stress within the cardiovascular environment are essential in the development of cardiovascular disease; however, the impact of such changes on the subcellular or organellar components and their functions that are relevant to cardiovascular disease inception are less understood. In this regard, studies are beginning to show that mitochondria not only appear susceptible to damage mediated by increased oxidative and nitrosoxidative stress, but also play significant roles in the regulation of cardiovascular cell function. In addition, accumulating evidence suggests that a common theme among cardiovascular disease development and cardiovascular disease risk factors is increased mitochondrial damage and dysfunction. This review discusses aspects relating mitochondrial damage and function to cardiovascular disease risk factors and disease development.
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“This results in increased cGMP concentrations in platelets, and this is thought to be the mechanism by which platelet function is inhibited (108,109) .”
From The effects of dietary nitrate on blood pressure and endothelial function: a review of human intervention studies (2013) · cites this paper as [109]
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“This results in increased cGMP concentrations in platelets, and this is thought to be the mechanism by which platelet function is inhibited (108,109) .”
From The effects of dietary nitrate on blood pressure and endothelial function: a review of human intervention studies (2013) · cites this paper as [109]
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Metadata
- Authors
- Ballinger, S. W.
- Affiliations
- University of Alabama at Birmingham (US)
- Corresponding author
- Ballinger, Scott W.
- ORCID
- Ballinger, Scott W.
- Venue
- Free Radical Biology and Medicine
- Publisher
- Elsevier BV
- Published
- 2005-05
- Volume
- 38
- Issue
- 10
- Pages
- 1278-1295
- ISSN
- 0891-5849 (ISSN-L)
- OpenAlex
- W2005139390
- Cited by
- 405
- References
- 222
- Citations by year
- 2026: 8 · 2025: 16 · 2024: 21 · 2023: 18 · 2022: 19 · 2021: 27 · 2020: 20 · 2019: 16 · 2018: 17 · 2017: 24 · 2016: 20 · 2015: 22 · 2014: 28 · 2013: 29 · 2012: 25
- FWCI
- 1.16
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Free Radical Biology and Medicine (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institutes of Health
- National Heart, Lung, and Blood Institute (HL 77419, R01HL077419)
- National Institute of Environmental Health Sciences (ES11172, R01ES011172)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
- Health Sciences › Medicine › Physiology (medical) › Nitric Oxide and Endothelin Effects
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiac Ischemia and Reperfusion
- Keywords
- mitochondrial dysfunction, mitochondrial damage, cardiovascular disease, atherosclerosis, oxidative stress, cardiovascular risk factors
- MeSH terms
- Animals, Cardiovascular Diseases, Humans, Mitochondria, Heart, Reactive Oxygen Species, Oxidative Stress
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.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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