The DOI matches its Crossref record; 225 of the 225 references it cites were found in a registry or an index.
Reactive oxygen species, cellular redox systems, and apoptosis
Open accessAbstract
Reactive oxygen species (ROS) are products of normal metabolism and xenobiotic exposure, and depending on their concentration, ROS can be beneficial or harmful to cells and tissues. At physiological low levels, ROS function as "redox messengers" in intracellular signaling and regulation, whereas excess ROS induce oxidative modification of cellular macromolecules, inhibit protein function, and promote cell death. Additionally, various redox systems, such as the glutathione, thioredoxin, and pyridine nucleotide redox couples, participate in cell signaling and modulation of cell function, including apoptotic cell death. Cell apoptosis is initiated by extracellular and intracellular signals via two main pathways, the death receptor- and the mitochondria-mediated pathways. Various pathologies can result from oxidative stress-induced apoptotic signaling that is consequent to ROS increases and/or antioxidant decreases, disruption of intracellular redox homeostasis, and irreversible oxidative modifications of lipid, protein, or DNA. In this review, we focus on several key aspects of ROS and redox mechanisms in apoptotic signaling and highlight the gaps in knowledge and potential avenues for further investigation. A full understanding of the redox control of apoptotic initiation and execution could underpin the development of therapeutic interventions targeted at oxidative stress-associated disorders.
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“ROS are highly chemically reactive molecules, derived from the deficient reduction in molecular oxygen (O2) and playing a critical role as signaling molecules in tumorigenesis [68], including asbestos-mediated carcinogenesis [15,66,69].”
From Chronic Inflammation, Oxidative Stress and Metabolic Plasticity: Three Players Driving the Pro-Tumorigenic Microenvironment in Malignant Mesothelioma (2023) · cites this paper as [69]
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Activation of apoptosis signalling pathways by reactive oxygen species
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Kurutas, E. B. (2015) · Nutrition Journal · doi:10.1186/s12937-016-0186-5 · Cited by 2,152
Oxidative stress: the mitochondria-dependent and mitochondria-independent pathways of apoptosis
Sinha, K., Das, J., Pal, P. B., & Sil, P. C. (2013) · Archives of Toxicology · doi:10.1007/s00204-013-1034-4 · Cited by 1,639
Colorectal Carcinoma: A General Overview and Future Perspectives in Colorectal Cancer
Mármol, I., Sánchez‐de‐Diego, C., Pradilla-Dieste, A., Cerrada, E., & Yoldi, M. R. (2017) · International Journal of Molecular Sciences · doi:10.3390/ijms18010197 · Cited by 1,632
Metadata
- Authors
- Circu, M. L., & Aw, T. Y.
- Affiliations
- Louisiana State University Health Sciences Center Shreveport (US)
- Corresponding author
- Aw, Tak Yee
- ORCID
- Circu, Magdalena L.
- Venue
- Free Radical Biology and Medicine
- Publisher
- Elsevier BV
- Published
- 2010-03
- Volume
- 48
- Issue
- 6
- Pages
- 749-762
- ISSN
- 0891-5849 (ISSN-L)
- PMC
- PMC2823977
- OpenAlex
- W1977178308
- Cited by
- 3,340
- References
- 224
- Citations by year
- 2026: 116 · 2025: 134 · 2024: 154 · 2023: 190 · 2022: 262 · 2021: 243 · 2020: 243 · 2019: 298 · 2018: 264 · 2017: 287 · 2016: 240 · 2015: 217 · 2014: 210 · 2013: 163 · 2012: 152
- FWCI
- 13.45
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Free Radical Biology and Medicine (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institutes of Health
- National Institute of Diabetes and Digestive and Kidney Diseases (R01DK044510, DK 44510)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Redox biology and oxidative stress
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Cell death mechanisms and regulation
- Health Sciences › Medicine › Biochemistry (medical) › Antioxidant Activity and Oxidative Stress
- Keywords
- reactive oxygen species, apoptosis, oxidative stress, redox signaling, glutathione, thioredoxin, pyridine nucleotides, death receptor signaling, mitochondrial apoptosis, antioxidant deficiency, redox homeostasis
- MeSH terms
- Animals, Humans, Oxidation-Reduction, Signal Transduction, Apoptosis, Reactive Oxygen Species
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