ReviewFree radical biology & medicine2012
The redox stress hypothesis of aging.
Review in Free radical biology & medicine, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 206 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
206 citing papers in PubMed, 469 citations in OpenAlex.
- Effects of Moderate Aerobic Exercise on Cognitive Abilities and Redox State Biomarkers in Older Adults.Oxidative medicine and cellular longevity · 2016Trial
- In Vivo Antioxidant Properties of Lotus Root and Cucumber: A Pilot Comparative Study in Aged Subjects.The journal of nutrition, health & aging · 2015Trial
- Reducing occupational stress with a B-vitamin focussed intervention: a randomized clinical trial: study protocol.Nutrition journal · 2014Trial
- Postprandial oxidative stress is modulated by dietary fat in adipose tissue from elderly people.Age (Dordrecht, Netherlands) · 2014Trial
- The gut microbiome and mitochondrial function in metabolism, immunity, and disease.Gut microbes · 2026Review
- Aged Mitochondrial DNA Is Associated With Aberrant Acute Exercise-Induced Redox Responses in Human Skeletal Muscle.Aging cell · 2026Article
- Tuning the Fire: Context-Dependent Mitochondrial ROS Signaling, Mitohormesis, and Redox-Modulating Interventions.Biomolecules · 2026Review
- The aging paradox of Cushing's syndrome: Stress without clear senescence?Journal of neuroendocrinology · 2026Review
- Oxidative stress causes a reversible decrease of deubiquitylases activity in old vertebrate brains.Nature communications · 2026Article
- Sulforaphane improves exercise-induced NRF2 signaling in older adults: an in vivo-ex vivo approach.GeroScience · 2026Article
- Article
- 3,5-Dicaffeoylquinic Acid Delayed Aging and Promoted Oxidative Stress Tolerance via Activation of the SKN-1/Nrf2 Signaling Pathway.Food science & nutrition · 2026Article
- Reactive Oxygen Species: Molecular Mechanisms, Cellular Targets, and Implications for Genomic Stability.BioMed research international · 2026Review
- Lifetime Deletion of Skeletal Muscle Keap1 Attenuates Aging-Induced Cardiac Dysfunction via an Nrf2-Antioxidant Mechanism.Antioxidants (Basel, Switzerland) · 2025Article
- Protective Role of p66Shc Deletion in Physiological Renal Aging: Effects on G Protein-Coupled Receptor 124 Expression and Associated Cellular Senescence.International journal of molecular sciences · 2025Article
- The Impairment of Body Condition Transiently Increases Oxidative Stress: A Dietary Restriction Experiment in Partridges.Journal of experimental zoology. Part A, Ecological and integrative physiology · 2025Article
- Article
- Pomegranate Extract Modulates Oxidative Stress by Reducing Basal ROS Levels and Protecting White Blood Cells from Induced Oxidative Damage in Aging Mice.International journal of molecular sciences · 2025Article
- Antioxidants in Age-Related Macular Degeneration: Lights and Shadows.Antioxidants (Basel, Switzerland) · 2025Review
- Knockdown of zebrafish tmem242 enhances the production of ROS that signals to increase f9a expression resulting in DIC-like condition.Scientific reports · 2025Article
146 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 2 institutions in 1 country.
Funding
Abstract
The main objective of this review is to examine the role of endogenous reactive oxygen/nitrogen species (ROS) in the aging process. Until relatively recently, ROS were considered to be potentially toxic by-products of aerobic metabolism, which, if not eliminated, may inflict structural damage on various macromolecules. Accrual of such damage over time was postulated to be responsible for the physiological deterioration in the postreproductive phase of life and eventually the death of the organism. This "structural damage-based oxidative stress" hypothesis has received support from the age-associated increases in the rate of ROS production and the steady-state amounts of oxidized macromolecules; however, there are increasing indications that structural damage alone is insufficient to satisfactorily explain the age-associated functional losses. The level of oxidative damage accrued during aging often does not match the magnitude of functional losses. Although experimental augmentation of antioxidant defenses tends to enhance resistance to induced oxidative stress, such manipulations are generally ineffective in the extension of life span of long-lived strains of animals. More recently, in a major conceptual shift, ROS have been found to be physiologically vital for signal transduction, gene regulation, and redox regulation, among others, implying that their complete elimination would be harmful. An alternative notion, advocated here, termed the "redox stress hypothesis," proposes that aging-associated functional losses are primarily caused by a progressive pro-oxidizing shift in the redox state of the cells, which leads to the overoxidation of redox-sensitive protein thiols and the consequent disruption of the redox-regulated signaling mechanisms.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.