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

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

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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Crossref · 10.1089/ars.2012.4604

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  • ATR1 also increases reactive oxygen species from mitochondria in monocytes/macrophages leading to DNA damage and apoptosis of T cells resulting in endothelial injury and lymphopenia.

    “ATR1 also increases reactive oxygen species from mitochondria in monocytes/macrophages leading to DNA damage and apoptosis of T cells resulting in endothelial injury and lymphopenia.”

    From COVID-19, Myocarditis and Pericarditis (2023) · cites this paper as [60]

    The Introduction describes AT1R-dependent mitochondrial ROS production, and the Conclusions link AngII-related mitochondrial dysfunction to endothelial dysfunction (page numbers unavailable). Neither passage supports the claimed sequence in which ROS from monocytes or macrophages causes T-cell DNA damage and apoptosis, endothelial injury, and lymphopenia. (LLM, conf=0.86)

    Experimental — accuracy not yet measured
  • The rescue of ANGII-induced cerebrovascular dysfunction by Nox2 deletion in PVMs was incomplete, possibly implicating ROS sources other than NOX2.

    “However, the rescue of the dysfunction was not complete, possibly implicating ROS sources other than NOX2 (33).”

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Authors
Dikalov, S. I., & Nazarewicz, R. R.
Affiliations
Vanderbilt University Medical Center (US)
Venue
Antioxidants & Redox Signaling
Published
2013-10
Volume
19
Issue
10
Pages
1085-1094
ISSN
  • 1523-0864 (ISSN-L)
  • 1557-7716
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 · 2012: 2
FWCI
1.36
Type
journal article
Language
en
Open access
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 › 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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