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.
Overview
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Integrity signals
Registry
Cites
Statistics
Verification
Claims the paper makes
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Claims other papers make about this one
Each is checked against this paper’s own text: does it say what the citing paper says it does?
The source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“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]
Experimental — accuracy not yet measured
Self-check
Percentages, sums and reported differences re-computed from the paper’s own numbers.
The self-check needs the paper’s full text.
Citations
Cites
The NOX Family of ROS-Generating NADPH Oxidases: Physiology and Pathophysiology
Bedard, K., & Krause, K.-H. (2007) · Physiological Reviews · doi:10.1152/physrev.00044.2005 · Cited by 6,989
Oxidants, antioxidants, and the degenerative diseases of aging.
Ames, B. N., Shigenaga, M. K., & Hagen, T. M. (1993) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.90.17.7915 · Cited by 5,958
Meister, A., & Anderson, M. E. (1983) · Annual Review of Biochemistry · doi:10.1146/annurev.bi.52.070183.003431 · Cited by 5,694
Mitochondrial formation of reactive oxygen species
Turrens, J. F. (2003) · The Journal of Physiology · doi:10.1113/jphysiol.2003.049478 · Cited by 5,084
Schafer, F. Q., & Buettner, G. R. (2001) · Free Radical Biology and Medicine · doi:10.1016/s0891-5849(01)00480-4 · Cited by 4,587
Molecular characterization of mitochondrial apoptosis-inducing factor
Susin, S. A., Lorenzo, H. K., Zamzami, N., Marzo, I., Snow, B. E., Brothers, G. M., Mangion, J., Jacotot, E., Costantini, P., Loeffler, M., et al. (1999) · Nature · doi:10.1038/17135 · Cited by 4,060
Du, C., Fang, M., Li, Y., Li, L., & Wang, X. (2000) · Cell · doi:10.1016/s0092-8674(00)00008-8 · Cited by 3,513
Stress-dependent regulation of FOXO transcription factors by the SIRT1 deacetylase
Brunet, A., Sweeney, L. B., Sturgill, J. F., Chua, K. F., Greer, P. L., Lin, Y., Tran, H., Ross, S. E., Mostoslavsky, R., Cohen, H. Y., et al. (2004) · Science · doi:10.1126/science.1094637 · Cited by 3,239
Induction of TNF receptor I-mediated apoptosis via two sequential signaling complexes
Micheau, O., & Tschopp, J. (2003) · Cell · doi:10.1016/s0092-8674(03)00521-x · Cited by 2,738
Structure, mechanism and regulation of peroxiredoxins
Wood, Z. A., Schröder, E., Harris, J. R., & Poole, L. B. (2003) · Trends in Biochemical Sciences · doi:10.1016/s0968-0004(02)00003-8 · Cited by 2,546
Cited by
Sorted by citations
Items 1,001–1,006 of 1,006
Fiorilla, I., Martinotti, S., Todesco, A. M., Bonsignore, G., Cavaletto, M., Patrone, M., Ranzato, E., & Audrito, V. (2023) · Cells · doi:10.3390/cells12162048 · Cited by 39
“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].”
BackgroundInvestigating the Effects of Stove Emissions on Ocular and Cancer Cells
Karakoçak, B. B., Patel, S., Ravi, N., & Biswas, P. (2019) · Scientific Reports · doi:10.1038/s41598-019-38803-4 · Cited by 26
ROS-responsive nanoparticle delivery of obeticholic acid mitigate primary sclerosing cholangitis
Yao, Q., Wang, B., Yu, J., Pan, Q., Yu, Y., Feng, X., Chen, W., Yang, J., Gao, C., & Cao, H. (2024) · Journal of Controlled Release · doi:10.1016/j.jconrel.2024.08.006 · Cited by 24
Korkmaz, Ş. A., Kızgın, S., Oğuz, E. F., Neşelioğlu, S., & Erel, Ö. (2023) · Journal of Affective Disorders · doi:10.1016/j.jad.2023.07.079 · Cited by 24
Zheng, W., Hu, J., Lv, Y., Bai, B., Shan, L., Chen, K., Dai, S., & Zhu, H. (2021) · Medical Oncology · doi:10.1007/s12032-021-01472-3 · Cited by 21
T cell tyrosine phosphorylation response to transient redox stress
Secchi, C., Carta, M., Crescio, C., Spano, A., Arras, M., Caocci, G., Galimi, F., La Nasa, G., Pippia, P., Turrini, F., et al. (2015) · Cellular Signalling · doi:10.1016/j.cellsig.2014.12.014 · Cited by 10
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
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
Are you an author, or do you see a problem with this page? Request a review
