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Mitochondrial Oxidative Stress Mediates Angiotensin II–Induced Cardiac Hypertrophy and Gαq Overexpression–Induced Heart Failure
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Rationale: Mitochondrial dysfunction has been implicated in several cardiovascular diseases; however, the roles of mitochondrial oxidative stress and DNA damage in hypertensive cardiomyopathy are not well understood. Objective: We evaluated the contribution of mitochondrial reactive oxygen species (ROS) to cardiac hypertrophy and failure by using genetic mouse models overexpressing catalase targeted to mitochondria and to peroxisomes. Methods and Results: Angiotensin II increases mitochondrial ROS in cardiomyocytes, concomitant with increased mitochondrial protein carbonyls, mitochondrial DNA deletions, increased autophagy and signaling for mitochondrial biogenesis in hearts of angiotensin II–treated mice. The causal role of mitochondrial ROS in angiotensin II–induced cardiomyopathy is shown by the observation that mice that overexpress catalase targeted to mitochondria, but not mice that overexpress wild-type peroxisomal catalase, are resistant to cardiac hypertrophy, fibrosis and mitochondrial damage induced by angiotensin II, as well as heart failure induced by overexpression of Gαq. Furthermore, primary damage to mitochondrial DNA, induced by zidovudine administration or homozygous mutation of mitochondrial polymerase γ, is also shown to contribute directly to the development of cardiac hypertrophy, fibrosis and failure. Conclusions: These data indicate the critical role of mitochondrial ROS in cardiac hypertrophy and failure and support the potential use of mitochondrial-targeted antioxidants for prevention and treatment of hypertensive cardiomyopathy.
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“Various signs of increased oxidative stress have been reported in various cardiovascular-related diagnoses such as heart failure (Dai et al. 2012), ventricular hypertrophy (Dai et al. 2011), myocardial infarction (Merabet et al. 2012), diabetes (Anderson et al. 2009) and other conditions.”
From Reactive Oxygen Species, Toxicity, Oxidative Stress, and Antioxidants: Chronic Diseases and Aging (2023) · cites this paper as Dai et al. 2011
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Metadata
- Authors
- Dai, D.-F., Johnson, S. C., Villarin, J. J., Chin, M. T., Nieves-Cintrón, M., Chen, T., Marcinek, D. J., Dorn, G. W., Kang, Y. J., Prolla, T. A., Santana, L. F., & Rabinovitch, P. S.
- Affiliations
- University of Louisville (US)
- From the Departments of Pathology (D.-F.D., S.C.J., T.C., P.S.R.), Radiology (J.J.V., D.J.M.), Cardiovascular Medicine (M.T.C.), Physiology and Biophysics (M.N.-C., L.F.S.), University of Washington, Seattle; Department of Internal Medicine (G.W.D.), Washington University School of Medicine, St Louis, MO; Departments of Medicine and Pharmacology and Toxicology (Y.J.K.), University of Louisville School of Medicine, KY; and Department of Genetics and Medical Genetics (T.A.P.), University of...
- ORCID
- Venue
- Circulation Research
- Published
- 2011-04
- Volume
- 108
- Issue
- 7
- Pages
- 837-846
- ISSN
- 0009-7330 (ISSN-L)
- 1524-4571
- PMC
- PMC3785241
- OpenAlex
- W2117205119
- Cited by
- 527
- References
- 35
- Citations by year
- 2026: 14 · 2025: 35 · 2024: 30 · 2023: 32 · 2022: 28 · 2021: 42 · 2020: 46 · 2019: 34 · 2018: 31 · 2017: 29 · 2016: 44 · 2015: 34 · 2014: 37 · 2013: 36 · 2012: 41
- FWCI
- 16.21
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Circulation Research (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institutes of Health (AG001751, AG013280)
- National Institute on Aging (AG-028455, AG001751, P01AG001751, AG013280, AG035844, RC1AG035844, R01AG028455, P30AG013280)
- National Heart, Lung, and Blood Institute (R01HL101186, HL-101186, R01HL063760, HL063760, R01HL059888)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiac Fibrosis and Remodeling
- Health Sciences › Medicine › Physiology (medical) › Nitric Oxide and Endothelin Effects
- Keywords
- mitochondrial oxidative stress, reactive oxygen species, angiotensin II, cardiac hypertrophy, heart failure, catalase, mitochondrial DNA damage, mitochondrial DNA deletions, autophagy, mitochondrial biogenesis, hypertensive cardiomyopathy, myocardial fibrosis, zidovudine, mitochondria-targeted antioxidants
- MeSH terms
- Angiotensin II, Animals, Catalase, DNA Damage, DNA, Mitochondrial, Gene Expression Regulation, Cardiomegaly, Heart Failure, Mice, Transgenic, Mitochondria, Heart, Zidovudine, Reactive Oxygen Species, Oxidative Stress, Reverse Transcriptase Inhibitors, Models, Animal, Myocytes, Cardiac, GTP-Binding Protein alpha Subunits, Gq-G11, Mice
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