Evidence map›Paper›PMID 38911254›Full record

ReviewOpen medicine (Warsaw, Poland)2024

Investigating hormesis, aging, and neurodegeneration: From bench to clinics.

Vittorio Calabrese, Uwe Wenzel, Tommaso Piccoli, Ursula M Jacob, Lidia Nicolosi, Giovanni Fazzolari, Gabriella Failla, Tilman Fritsch, Naomi Osakabe, Edward J Calabrese

Erratum issuedAbstract readReview
In one paragraph

Review in Open medicine (Warsaw, Poland), 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

12 citing papers in PubMed.

  1. Trial
  2. Article
  3. Review
  4. Review
  5. Article
  6. Article
  7. Redox Homeostasis in Poultry/Animal Production.Antioxidants (Basel, Switzerland) · 2025
    Article
  8. Article
  9. Oxytocin, Vasopressin and Stress: A Hormetic Perspective.Current issues in molecular biology · 2025
    Review
  10. Review
  11. Article
  12. Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

10 authors.

Vittorio CalabreseDepartment of Biomedical and Biotechnological Sciences, University of Catania, Catania, Italy.
Uwe WenzelInstitut für Ernährungswissenschaft, Justus Liebig Universitat Giessen, Germany.
Tommaso PiccoliNeurology Unit, Department of Biomedicine, Neuroscience and Advanced Diagnostics (BIND), University of Palermo, Palermo, Italy.
Ursula M JacobSystem Biologie AG, Wollerau, Switzerland.
Lidia NicolosiDepartment of Biomedical and Biotechnological Sciences, University of Catania, Catania, Italy.
Giovanni FazzolariDepartment of Biomedical and Biotechnological Sciences, University of Catania, Catania, Italy.
Gabriella FaillaDepartment of Biomedical and Biotechnological Sciences, University of Catania, Catania, Italy.
Tilman FritschNAM Institute, Salzburg, Austria.
Naomi OsakabeDepartment of Bio-Science and Engineering, Faculty of System Science and Engineering, Shibaura Institute of Technology, Tokyo, Japan.
Edward J CalabreseDepartment of Environmental Health Sciences, Morrill I, N344, University of Massachusetts, Amherst, MA 01003, United States of America.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Mitochondria-derived reactive oxygen species production at a moderate physiological level plays a fundamental role in the anti-aging signaling, due to their action as redox-active sensors for the maintenance of optimal mitochondrial balance between intracellular energy status and hormetic nutrients. Iron regulatory protein dysregulation, systematically increased iron levels, mitochondrial dysfunction, and the consequent oxidative stress are recognized to underlie the pathogenesis of multiple neurodegenerative diseases, such as Parkinson's disease and Alzheimer's disease. Central to their pathogenesis, Nrf2 signaling dysfunction occurs with disruption of metabolic homeostasis. We highlight the potential therapeutic importance of nutritional polyphenols as substantive regulators of the Nrf2 pathway. Here, we discuss the common mechanisms targeting the Nrf2/vitagene pathway, as novel therapeutic strategies to minimize consequences of oxidative stress and neuroinflammation, generally associated to cognitive dysfunction, and demonstrate its key neuroprotective and anti-neuroinflammatory properties, summarizing pharmacotherapeutic aspects relevant to brain pathophysiology.

Indexed as

antioxidantsC. eleganshormesislongevitymitochondrial medicineNrf2

Identifiers

PMID38911254
PMCPMC11193355

What OpenQuestion holds

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Registered trials

None linked

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.