ReviewAging2011
Hormesis, cell death and aging.
Review in Aging, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 68 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
68 citing papers in PubMed, 127 citations in OpenAlex.
- Molecular Insights into the Genesis of Heat Hardening in Marine Bivalves.Antioxidants (Basel, Switzerland) · 2025Article
- Cytotoxic effect of 3D-printed and thermoformed clear aligner materials on human oral fibroblasts: AnKorean journal of orthodontics · 2025Article
- ER stress tolerance is regulated by copper-dependent PERK kinase activity.Cell reports · 2025Article
- Article
- Unlocking the Power: New Insights into the Anti-Aging Properties of Mushrooms.Journal of fungi (Basel, Switzerland) · 2024Review
- Persistent elevation of plasma markers of cellular senescence after hip fracture: a pilot longitudinal study.Frontiers in aging · 2024Article
- Quantum Electrodynamics Coherence and Hormesis: Foundations of Quantum Biology.International journal of molecular sciences · 2023Review
- House ammonia exposure causes alterations in microbiota, transcriptome, and metabolome of rabbits.Frontiers in microbiology · 2023Article
- Review
- Artemisinin relieves osteoarthritis by activating mitochondrial autophagy through reducing TNFSF11 expression and inhibiting PI3K/AKT/mTOR signaling in cartilage.Cellular & molecular biology letters · 2022Article
- Article
- Activation of immune cell proteasomes in peripheral blood of smokers and COPD patients: implications for therapy.The European respiratory journal · 2022Article
- PLGA-Based Curcumin Delivery System: An Interesting Therapeutic Approach in the Treatment of Alzheimer's Disease.Current neuropharmacology · 2022Review
- Increased oxidative stress during exercise predicts poor prognosis in patients with acute decompensated heart failure.ESC heart failure · 2021Article
- Autophagy in major human diseases.The EMBO journal · 2021Review
- Myocardial perfusion imaging with cadmium-zinc-telluride cameras: Harry Potter and the Radiation Hallows?Journal of nuclear cardiology : official publication of the American Society of Nuclear Cardiology · 2021Article
- Article
- Mitochondrial Toxins and Healthy Lifestyle Meet at the Crossroad of Hormesis.Diabetes & metabolism journal · 2019Review
- New approaches to cope with possible harms of low-dose environmental chemicals.Journal of epidemiology and community health · 2019Article
- The Naked Mole Rat: A Unique Example of Positive Oxidative Stress.Oxidative medicine and cellular longevity · 2019Review
8 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
3 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Frequently, low doses of toxins and other stressors not only are harmless but also activate an adaptive stress response that raise the resistance of the organism against high doses of the same agent. This phenomenon, which is known as "hormesis", is best represented by ischemic preconditioning, the situation in which short ischemic episodes protect the brain and the heart against prolonged shortage of oxygen and nutrients. Many molecules that cause cell death also elicit autophagy, a cytoprotective mechanism relying on the digestion of potentially harmful intracellular structures, notably mitochondria. When high doses of these agents are employed, cells undergo mitochondrial outer membrane permeabilization and die. In contrast, low doses of such cytotoxic agents can activate hormesis in several paradigms, and this may explain the lifespan-prolonging potential of autophagy inducers including resveratrol and caloric restriction.
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.