ReviewRedox biology2014
Positive oxidative stress in aging and aging-related disease tolerance.
Review in Redox biology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 94 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
94 citing papers in PubMed.
- Chemical generation of superoxide in the co-presence of riboflavin derivatives and NADH: evidence for a non-enzymatic redox pathway.Journal of clinical biochemistry and nutrition · 2026Article
- Phytochemicals and REDOX Modulation: Molecular Mechanisms, Clinical Relevance, and Therapeutic Perspectives.Antioxidants (Basel, Switzerland) · 2026Review
- Article
- Role of Antioxidants in Diseases and its Impact on Mitochondria with A Focus on Diabetes: An Overview.Current drug research reviews · 2026Review
- Mitochondrial dysfunction in perimenopausal mood disorders: From hormonal shifts to neuroenergetic failure (Review).International journal of molecular medicine · 2025Review
- The molecular determinants regulating redox signaling in diabetic endothelial cells.Frontiers in pharmacology · 2025Review
- Iron oxide nanoparticles induce ferroptosis under mild oxidative stress in vitro.Scientific reports · 2024Article
- Article
- Up-regulated succinylation modifications induce a senescence phenotype in microglia by altering mitochondrial energy metabolism.Journal of neuroinflammation · 2024Article
- Mapping the evolution of liver aging research: A bibliometric analysis.World journal of gastroenterology · 2024Article
- Total flavonoids ofIranian journal of basic medical sciences · 2024Article
- Mitochondrial dysfunction and its association with age-related disorders.Frontiers in physiology · 2024Review
- Oxidative eustress: the physiological role of oxidants.Science China. Life sciences · 2023Article
- Age-Related Changes in Post-Translational Modifications of Proteins from Whole Male and Female Skeletal Elements.Molecules (Basel, Switzerland) · 2023Article
- Dietary intake of microplastics impairs digestive performance, induces hepatic dysfunction, and shortens lifespan in the annual fish Nothobranchius guentheri.Biogerontology · 2023Article
- Cellular rejuvenation: molecular mechanisms and potential therapeutic interventions for diseases.Signal transduction and targeted therapy · 2023Review
- Review
- Radiation as a Tool against Neurodegeneration-A Potential Treatment for Amyloidosis in the Central Nervous System.International journal of molecular sciences · 2022Review
- Metformin's Mechanisms in Attenuating Hallmarks of Aging and Age-Related Disease.Aging and disease · 2022Article
- Article
34 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
Abstract
It is now well established that reactive oxygen species (ROS), reactive nitrogen species (RNS), and a basal level of oxidative stress are essential for cell survival. It is also well known that while severe oxidative stress often leads to widespread oxidative damage and cell death, a moderate level of oxidative stress, induced by a variety of stressors, can yield great beneficial effects on adaptive cellular responses to pathological challenges in aging and aging-associated disease tolerance such as ischemia tolerance. Here in this review, I term this moderate level of oxidative stress as positive oxidative stress, which usually involves imprinting molecular signatures on lipids and proteins via formation of lipid peroxidation by-products and protein oxidation adducts. As ROS/RNS are short-lived molecules, these molecular signatures can thus execute the ultimate function of ROS/RNS. Representative examples of lipid peroxidation products and protein oxidation adducts are presented to illustrate the role of positive oxidative stress in a variety of pathological settings, demonstrating that positive oxidative stress could be a valuable prophylactic and/or therapeutic approach targeting aging and aging-associated diseases.
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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.