Mitochondrial proteome remodelling in pressure overload-induced heart failure: the role of mitochondrial oxidative stress
Open accessAbstract
AIMS: We investigate the role of mitochondrial oxidative stress in mitochondrial proteome remodelling using mouse models of heart failure induced by pressure overload. METHODS AND RESULTS: We demonstrate that mice overexpressing catalase targeted to mitochondria (mCAT) attenuate pressure overload-induced heart failure. An improved method of label-free unbiased analysis of the mitochondrial proteome was applied to the mouse model of heart failure induced by transverse aortic constriction (TAC). A total of 425 mitochondrial proteins were compared between wild-type and mCAT mice receiving TAC or sham surgery. The changes in the mitochondrial proteome in heart failure included decreased abundance of proteins involved in fatty acid metabolism, an increased abundance of proteins in glycolysis, apoptosis, mitochondrial unfolded protein response and proteolysis, transcription and translational control, and developmental processes as well as responses to stimuli. Overexpression of mCAT better preserved proteins involved in fatty acid metabolism and attenuated the increases in apoptotic and proteolytic enzymes. Interestingly, gene ontology analysis also showed that monosaccharide metabolic processes and protein folding/proteolysis were only overrepresented in mCAT but not in wild-type mice in response to TAC. CONCLUSION: This is the first study to demonstrate that scavenging mitochondrial reactive oxygen species (ROS) by mCAT not only attenuates most of the mitochondrial proteome changes in heart failure, but also induces a subset of unique alterations. These changes represent processes that are adaptive to the increased work and metabolic requirements of pressure overload, but which are normally inhibited by overproduction of mitochondrial ROS.
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Various signs of increased oxidative stress have been reported in heart failure, ventricular hypertrophy, myocardial infarction, diabetes, and other conditions.
“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. 2012
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- Authors
- Dai, D.-F., Hsieh, E. J., Liu, Y., Chen, T., Beyer, R. P., Chin, M. T., MacCoss, M. J., & Rabinovitch, P. S.
- Affiliations
- University of Washington (US)
- Corresponding author
- Rabinovitch, Peter S.
- Venue
- Cardiovascular Research
- Publisher
- Oxford University Press (OUP)
- Published
- 2011-10-19
- Volume
- 93
- Issue
- 1
- Pages
- 79-88
- ISSN
- 0008-6363 (ISSN-L)
- 1755-3245
- PMC
- PMC3243039
- OpenAlex
- W2163954402
- Cited by
- 178
- References
- 33
- Citations by year
- 2026: 8 · 2025: 6 · 2024: 11 · 2023: 13 · 2022: 8 · 2021: 16 · 2020: 13 · 2019: 6 · 2018: 13 · 2017: 20 · 2016: 15 · 2015: 13 · 2014: 18 · 2013: 7 · 2012: 11
- FWCI
- 4.67
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Cardiovascular Research (publishedVersion)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institutes of Health (AG013280)
- National Institute on Aging (P01AG001751, AG013280, AG000751, P30AG013280)
- National Heart, Lung, and Blood Institute (R01HL101186, HL-101186)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
- Health Sciences › Medicine › Pathology and Forensic Medicine › Cardiac Ischemia and Reperfusion
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiac Fibrosis and Remodeling
- Keywords
- mitochondrial oxidative stress, catalase overexpression, transverse aortic constriction, mitochondrial reactive oxygen species, fatty acid metabolism, apoptosis, proteolysis, mitochondrial unfolded protein response, protein folding
- MeSH terms
- Animals, Catalase, Disease Models, Animal, Heart Failure, Mice, Inbred C57BL, Mice, Transgenic, Mitochondria, Heart, Oxidative Stress, Proteome, Mitochondrial Proteins, Mice
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