The DOI matches its Crossref record; 68 of the 68 references it cites were found in a registry or an index.
Angiotensin II-Induced Production of Mitochondrial Reactive Oxygen Species: Potential Mechanisms and Relevance for Cardiovascular Disease
Open accessAbstract
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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“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]
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“However, the rescue of the dysfunction was not complete, possibly implicating ROS sources other than NOX2 (33).”
From Perivascular macrophages mediate the neurovascular and cognitive dysfunction associated with hypertension (2016) · cites this paper as [33]
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1 retracted
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The Pathobiology of Diabetic Complications
Brownlee, M. (2005) · Diabetes · doi:10.2337/diabetes.54.6.1615 · Cited by 5,339
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Lambeth, J. D. (2004) · Nature Reviews Immunology · doi:10.1038/nri1312 · Cited by 3,125
NAD(P)H Oxidase: Role in Cardiovascular Biology and Disease
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Mitochondrial Dysfunction in Atherosclerosis
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Functional analysis of Nox4 reveals unique characteristics compared to other NADPH oxidases
Martyn, K. D., Frederick, L. M., von Loehneysen, K., Dinauer, M. C., & Knaus, U. G. (2006) · Cellular Signalling · doi:10.1016/j.cellsig.2005.03.023 · Cited by 783
Cross talk between mitochondria and NADPH oxidases
Dikalov, S. (2011) · Free Radical Biology and Medicine · doi:10.1016/j.freeradbiomed.2011.06.033 · Cited by 783
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Angiotensin II Signal Transduction: An Update on Mechanisms of Physiology and Pathophysiology
Forrester, S. J., Booz, G. W., Sigmund, C. D., Coffman, T. M., Kawai, T., Rizzo, V., Scalia, R. G., & Eguchi, S. (2018) · Physiological Reviews · doi:10.1152/physrev.00038.2017 · Cited by 1,135
Mitochondrial dysfunction and oxidative stress in heart disease
Peoples, J. N., Saraf, A., Ghazal, N., Pham, T. T., & Kwong, J. Q. (2019) · Experimental & Molecular Medicine · doi:10.1038/s12276-019-0355-7 · Cited by 950
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Deng, T., Lyon, C. J., Bergin, S. M., Caligiuri, M. A., & Hsueh, W. A. (2016) · Annual Review of Pathology Mechanisms of Disease · doi:10.1146/annurev-pathol-012615-044359 · Cited by 831
Goette, A., Kalman, J. M., Aguinaga, L., Akar, J. G., Cabrera, J. Á., Chen, S. A., Chugh, S. S., Corradi, D., d’Ávila, A., Dobrev, D., et al. (2016) · Heart Rhythm · doi:10.1016/j.hrthm.2016.05.028 · Cited by 791
Metadata
- 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
- 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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