The DOI matches its Crossref record; 224 of the 224 references it cites were found in a registry or an index.
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]
In the citing paper
“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]
Citations
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Cited by
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Oxidative Stress, Prooxidants, and Antioxidants: The Interplay
Rahal, A., Kumar, A., Singh, V., Yadav, B., Tiwari, R., Chakraborty, S., & Dhama, K. (2014) · BioMed Research International · doi:10.1155/2014/761264 · Cited by 1,806
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Mitochondria and reactive oxygen species
Kowaltowski, A. J., de Souza-Pinto, N. C., Castilho, R. F., & Vercesi, A. E. (2009) · Free Radical Biology and Medicine · doi:10.1016/j.freeradbiomed.2009.05.004 · Cited by 1,162
Li, X., Fang, P., Mai, J., Choi, E. T., Wang, H., & Yang, X. (2013) · Journal of Hematology & Oncology · doi:10.1186/1756-8722-6-19 · Cited by 860
Endothelial dysfunction — A major mediator of diabetic vascular disease
Sena, C. M., Pereira, A. M., & Seiça, R. M. F. (2013) · Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease · doi:10.1016/j.bbadis.2013.08.006 · Cited by 819
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
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