Cited by 406Mitochondrial Function and PathologyNitric Oxide and Endothelin EffectsCardiac Ischemia and Reperfusion

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Mitochondrial dysfunction in cardiovascular disease

Ballinger, Scott W.·2005·Free Radical Biology and Medicine

DOI 10.1016/j.freeradbiomed.2005.02.014

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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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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)
DOI: 10.1016/j.freeradbiomed.2005.02.014
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
Licence: www.elsevier.com/tdm/userlicense/1.0/ (tdm)
www.elsevier.com/legal/tdmrep-license (tdm)
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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