Protein oxidation and cellular homeostasis: Emphasis on metabolism
Open accessAbstract
Reactive oxygen species (ROS) are generated as the result of a number of physiological and pathological processes. Once formed ROS can promote multiple forms of oxidative damage, including protein oxidation, and thereby influence the function of a diverse array of cellular processes. This review summarizes the mechanisms by which ROS are generated in a variety of cell types, outlines the mechanisms which control the levels of ROS, and describes specific proteins which are common targets of ROS. Additionally, this review outlines cellular processes which can degrade or repair oxidized proteins, and ultimately describes the potential outcomes of protein oxidation on cellular homeostasis. In particular, this review focuses on the relationship between elevations in protein oxidation and multiple aspects of cellular metabolism. Together, this review describes a potential role for elevated levels of protein oxidation contributing to cellular dysfunction and oxidative stress via impacts on cellular metabolism.
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ROS in excess can provoke energy stress and metabolic failure by directly oxidizing and inactivating enzymes of the tricarboxylic acid cycle, electron transport chain, and glycolysis.
“ROS, in excess, can provoke energy stress and metabolic failure by direct oxidizing and inactivating enzymes of the tricarboxylic acid cycle, electron transport chain (ETC), and glycolysis [62,63].”
From AMPK, Mitochondrial Function, and Cardiovascular Disease (2020) · cites this paper as [63]
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References 134 · Cited by 274
Research works printed but not linked: 1
- D.V. Voet Judith, Biochemistry, 3rd ed. Jon Wiley and Sons Inc, Hoboken, NJ, 2003.
- Authors
- Cecarini, V., Gee, J., Fioretti, E., Amici, M., Angeletti, M., Eleuteri, A. M., & Keller, J. N.
- Affiliations
- Università di Camerino (IT)
- University of Kentucky (US)
- Corresponding author
- Keller, Jeffrey N.
- Venue
- Biochimica et Biophysica Acta (BBA) - Molecular Cell Research
- Publisher
- Elsevier BV
- Published
- 2007-02
- Volume
- 1773
- Issue
- 2
- Pages
- 93-104
- ISSN
- 0167-4889 (ISSN-L)
- OpenAlex
- W2170591186
- Cited by
- 274
- References
- 134
- Citations by year
- 2026: 9 · 2025: 22 · 2024: 17 · 2023: 14 · 2022: 17 · 2021: 27 · 2020: 21 · 2019: 15 · 2018: 12 · 2017: 7 · 2016: 9 · 2015: 14 · 2014: 17 · 2013: 10 · 2012: 9
- FWCI
- 0.72
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- Biochimica et Biophysica Acta (BBA) - Molecular Cell Research (publishedVersion)
- PubMed (publishedVersion)
- Unicam Scientific Publications (University of Camerino) (submittedVersion)
- Funders
- Alzheimer's Association
- Università degli Studi di Camerino
- National Institutes of Health
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Redox biology and oxidative stress
- Health Sciences › Medicine › Biochemistry › Antioxidant Activity and Oxidative Stress
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Cancer and biochemical research
- Keywords
- protein oxidation, reactive oxygen species, cellular homeostasis, cellular metabolism, oxidative stress, reactive oxygen species generation, protein repair, protein degradation, cellular dysfunction
- MeSH terms
- Animals, Antioxidants, Homeostasis, Humans, Oxidation-Reduction, Protein Processing, Post-Translational, Proteins, Oxidative Stress
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