Cited by 356Nitric Oxide and Endothelin EffectsRenin-Angiotensin System StudiesRedox biology and oxidative stress

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Angiotensin II-Induced Production of Mitochondrial Reactive Oxygen Species: Potential Mechanisms and Relevance for Cardiovascular Disease

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Dikalov, Sergey I., Nazarewicz, Rafal R.·2013·Antioxidants & Redox Signaling

DOI 10.1089/ars.2012.4604PMC PMC3771548

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Abstract

SIGNIFICANCE: The role of reactive oxygen species (ROS) in angiotensin II (AngII) induced endothelial dysfunction, cardiovascular and renal remodeling, inflammation, and fibrosis has been well documented. The molecular mechanisms of AngII pathophysiological activity involve the stimulation of NADPH oxidases, which produce superoxide and hydrogen peroxide. AngII also increases the production of mitochondrial ROS, while the inhibition of AngII improves mitochondrial function; however, the specific molecular mechanisms of the stimulation of mitochondrial ROS is not clear. RECENT ADVANCES: Interestingly, the overexpression of mitochondrial thioredoxin 2 or mitochondrial superoxide dismutase attenuates AngII-induced hypertension, which demonstrates the importance of mitochondrial ROS in AngII-mediated cardiovascular diseases. CRITICAL ISSUES: Although mitochondrial ROS plays an important role in normal physiological cell signaling, AngII, high glucose, high fat, or hypoxia may cause the overproduction of mitochondrial ROS, leading to the feed-forward redox stimulation of NADPH oxidases. This vicious cycle may contribute to the development of pathological conditions and facilitate organ damage in hypertension, atherosclerosis, and diabetes. FUTURE DIRECTIONS: The development of antioxidant strategies specifically targeting mitochondria could be therapeutically beneficial in these disease conditions.

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Authors: Dikalov, S. I., & Nazarewicz, R. R.
Affiliations: Vanderbilt University Medical Center (US)
ORCID: Dikalov, Sergey I.
Venue: Antioxidants & Redox Signaling
Publisher: SAGE Publications
Published: 2013-10
Volume: 19
Issue: 10
Pages: 1085-1094
ISSN: 1523-0864 (ISSN-L)
1557-7716
DOI: 10.1089/ars.2012.4604
PMC: PMC3771548
OpenAlex: W2085076776
Cited by: 356
References: 68
Citations by year: 2026: 25 · 2025: 29 · 2024: 22 · 2023: 38 · 2022: 32 · 2021: 49 · 2020: 34 · 2019: 22 · 2018: 19 · 2017: 21 · 2016: 26 · 2015: 20 · 2014: 9 · 2013: 8
FWCI: 1.36
Type: journal article
Language: en
Open access: green
www.ncbi.nlm.nih.gov
Locations: Antioxidants and Redox Signaling (publishedVersion)
Europe PMC (PubMed Central) (publishedVersion)
PubMed Central (publishedVersion)
PubMed (publishedVersion)
Funders: National Heart, Lung, and Blood Institute (R01HL094469, HL094469)
Topics: Health Sciences › Medicine › Physiology (medical) › Nitric Oxide and Endothelin Effects
Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Renin-Angiotensin System Studies
Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Redox biology and oxidative stress
Keywords: angiotensin II, mitochondrial reactive oxygen species, NADPH oxidase, superoxide, hydrogen peroxide, thioredoxin 2, mitochondrial superoxide dismutase, hypertension, atherosclerosis, diabetes mellitus, endothelial dysfunction, renal remodeling, mitochondrial dysfunction, antioxidant therapy
MeSH terms: Angiotensin II, Animals, Cardiovascular Diseases, Humans, Hydrogen Peroxide, Mitochondria, Superoxide Dismutase, Signal Transduction, Reactive Oxygen Species, Oxidative Stress, NADPH Oxidases

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Angiotensin II-Induced Production of Mitochondrial Reactive Oxygen Species: Potential Mechanisms and Relevance for Cardiovascular Disease

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