Redox signaling: an evolution from free radicals to aging
Open accessAbstract
Redox biology has evolved from studies of the pathology that involves oxidants to an understanding of how oxidants participate in normal as well as aberrant signal transduction. Although the concept that signal transduction involved changes in the redox state dates from the 1930s, the modern history of redox biology began with the discovery of superoxide dismutase by McCord and Fridovich. The initial focus was on free radicals and damage of macromolecules, which remains an important topic. But, over time it was realized that hydroperoxides, especially H2O2 produced by NADPH oxidases, and electrophiles derived from lipid peroxidation or metabolism, played essential roles in physiologically relevant signaling. The mechanisms through which H2O2 and other electrophiles signal became an important area of study that provided insight into how these reactive molecules were involved in major signaling pathways and regulation of transcription factors. Thus, the field of redox signaling that is the overlap of signal transduction with redox biology was established. Alterations in redox signaling are observed in aging, but we also now know that redox signaling is essential in physiological homeostasis and that sustained deviation from redox homeostasis results in disease. This is a review of the history of redox biology from a personal perspective of nearly fifty years working in this field that hopefully provides some insights for the reader.
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Several types of SOD are present in the cytosol and mitochondria of human cells, where they convert O2•- into H2O2 and molecular oxygen.
“In addition, several types of SOD are present in the cytosol and in the mitochondria of human cells, where they convert O 2 •-into H 2 O 2 and molecular oxygen (O 2 ) [164].”
From Sunlight damage to cellular DNA: focus on oxidatively generated lesions (2017) · cites this paper as [164]
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Mutations of the Electron Transport Chain Affect Lifespan and ROS Levels in C. elegans
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- Authors
- Forman, H. J.
- Affiliations
- University of Southern California (US)
- Corresponding author
- Forman, Henry Jay
- ORCID
- Forman, Henry Jay
- Venue
- Free Radical Biology and Medicine
- Publisher
- Elsevier BV
- Published
- 2016-08
- Volume
- 97
- Pages
- 398-407
- ISSN
- 0891-5849 (ISSN-L)
- PMC
- PMC4996735
- OpenAlex
- W2417395786
- Cited by
- 172
- References
- 121
- Citations by year
- 2026: 7 · 2025: 15 · 2024: 18 · 2023: 15 · 2022: 19 · 2021: 13 · 2020: 19 · 2019: 17 · 2018: 16 · 2017: 27 · 2016: 6
- FWCI
- 1.99
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Free Radical Biology and Medicine (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institutes of Health
- NIH (ES023864)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Redox biology and oxidative stress
- Health Sciences › Medicine › Biochemistry › Antioxidant Activity and Oxidative Stress
- Health Sciences › Medicine › Physiology › Nitric Oxide and Endothelin Effects
- Keywords
- redox signaling, redox biology, free radicals, superoxide dismutase, hydrogen peroxide, NADPH oxidase, hydroperoxides, electrophiles, lipid peroxidation, signal transduction, transcription factor regulation, aging, redox homeostasis
- MeSH terms
- Animals, Free Radicals, Gene Expression Regulation, Homeostasis, Humans, Lipid Peroxidation, Signal Transduction, Oxidative Stress
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