ArticleAntioxidants & redox signaling2014
The free radical theory of aging is dead. Long live the damage theory!
Article in Antioxidants & redox signaling, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 134 papers, 3 of them syntheses that pooled it.
What it found
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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.
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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.
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Who cites it
134 citing papers in PubMed, 3 syntheses or guidelines pooled it.
- Dietary patterns and biomarkers of oxidative stress and inflammation: A systematic review of observational and intervention studies.Redox biology · 2021Pooled it
- Pooled it
- The Effect of MitoQ on Aging-Related Biomarkers: A Systematic Review and Meta-Analysis.Oxidative medicine and cellular longevity · 2018Pooled it
- Removal of aging microenvironment of bone defects can effectively promote bone defect repair.Journal of translational medicine · 2026Article
- GCN5L1-Mediated Lysine Acetylation Regulates Mitochondrial Bioenergetics and Redox Homeostasis in the Aged Heart.Antioxidants (Basel, Switzerland) · 2026Article
- Effects of storage conditions on oxidative stress biomarkers: methodological implications for ecological and evolutionary studies.The Journal of experimental biology · 2026Article
- Investigating the protective and therapeutic potential of new generation antioxidant combinations in the brain: an experimental aging model.Biogerontology · 2026Article
- The road to a long lifespan in the Persian squirrel, a natural model for extended longevity: resisting free radical stress and healthy phospholipids.GeroScience · 2026Article
- A mechanism for the disrupted redox regulation of vascular contractility during aging.iScience · 2026Article
- Mitochondrial respiration in peripheral blood mononuclear cells of healthy adult population.PloS one · 2026Article
- Reactive Oxygen Species: Molecular Mechanisms, Cellular Targets, and Implications for Genomic Stability.BioMed research international · 2026Review
- Redox Regulation of Complement Pathway Activation in Aging and Related Diseases.Antioxidants (Basel, Switzerland) · 2025Review
- Mitochondrial dysfunction in cellular senescence: a bridge to neurodegenerative disease.npj aging · 2025Review
- From Elixirs to Geroscience: A Historical and Molecular Perspective on Anti-Aging Medicine.Molecules (Basel, Switzerland) · 2025Review
- Targeting macro- and micro-nutrient regulation of HNeurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2025Review
- Involvement of NRF2 and AMPK signaling in aging and progeria: a digest.Redox biology · 2025Review
- Biomarkers of Oxidative and Mitochondrial Stress Are Associated With Accelerated Pace of Aging at Midlife in a Birth Cohort.The journals of gerontology. Series A, Biological sciences and medical sciences · 2025Article
- Article
- Copper Imparts a New Therapeutic Property to Resveratrol by Generating ROS to Deactivate Cell-Free Chromatin.Pharmaceuticals (Basel, Switzerland) · 2025Article
- Something Is Rotten in the State of Redox.Antioxidants (Basel, Switzerland) · 2025Article
74 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
1 author.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The free radical theory of aging posits that aging is caused by accumulation of damage inflicted by reactive oxygen species (ROS). Although this concept has been very useful in defining the contribution of oxidative damage to the aging process, an increasing number of studies contradict it. The idea that oxidative damage represents only one of many causes of aging also has limitations, as it does not explain causal relationships and inevitability of damage accumulation. Here, it is discussed that infidelity, heterogeneity, and imperfectness of each and every biological process may be responsible for the inevitable accumulation of by-products and other damage forms. Although ROS are prototypical by-products, their contribution to aging is governed by the metabolic organization of the cell, its protective systems, and genotype. These factors are controlled by natural selection and, like dietary and genetic interventions that extend lifespan, change the composition of cumulative damage and the rates of accumulation of its various forms. Oxidative damage, like other specific damage types viewed in isolation or in combination, does not represent the cause of aging. Instead, biological imperfectness, which leads to inevitable accumulation of damage in the form of mildly deleterious molecular species, may help define the true root of aging. Free radical and other specialized damage theories served their purpose in the understanding of the aging process, but in the current form they limit further progress in this area.
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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.