Cited by 3,340Redox biology and oxidative stressCell death mechanisms and regulationAntioxidant Activity and Oxidative Stress

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Reactive oxygen species, cellular redox systems, and apoptosis

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Circu, Magdalena L., Aw, Tak Yee·2010·Free Radical Biology and Medicine

DOI 10.1016/j.freeradbiomed.2009.12.022PMC PMC2823977

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Abstract

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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Retracted
The role and function of PPARγ in bladder cancer
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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)
DOI: 10.1016/j.freeradbiomed.2009.12.022
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
Licence: www.elsevier.com/tdm/userlicense/1.0/ (tdm)
www.elsevier.com/legal/tdmrep-license (tdm)
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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Reactive oxygen species, cellular redox systems, and apoptosis

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