Evidence map›Paper›PMID 26380578›Full record

ArticleImmunity & ageing : I & A2015

Hormetic effect of rotenone in primary human fibroblasts.

Shiva Marthandan, Steffen Priebe, Marco Groth, Reinhard Guthke, Matthias Platzer, Peter Hemmerich, Stephan Diekmann

Open access · goldAbstract read
In one paragraph

Article in Immunity & ageing : I & A, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
0.9field-weighted citation impact, top 25% of its field
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

18 citing papers in PubMed, 28 citations in OpenAlex.

  1. Article
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  5. A Redox-Shifted Fibroblast Subpopulation Emerges in the Fibrotic Lung.American journal of respiratory cell and molecular biology · 2024
    Article
  6. Article
  7. Review
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  9. Article
  10. The quest to define senescence.Frontiers in genetics · 2024
    Article
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  12. Review
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  14. Article
  15. Review
  16. Article
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

7 authors at 3 institutions in 1 country.

Shiva MarthandanLeibniz-Institute for Age Research - Fritz Lipmann Institute e.V. (FLI), Beutenbergstrasse 11, D-07745 Jena, Germany.
Steffen PriebeLeibniz Institute for Natural Product Research and Infection Biology - Hans-Knöll-Institute e.V. (HKI), Jena, Germany.
Marco GrothLeibniz-Institute for Age Research - Fritz Lipmann Institute e.V. (FLI), Beutenbergstrasse 11, D-07745 Jena, Germany.
Reinhard GuthkeLeibniz Institute for Natural Product Research and Infection Biology - Hans-Knöll-Institute e.V. (HKI), Jena, Germany.
Matthias PlatzerLeibniz-Institute for Age Research - Fritz Lipmann Institute e.V. (FLI), Beutenbergstrasse 11, D-07745 Jena, Germany.
Peter HemmerichLeibniz-Institute for Age Research - Fritz Lipmann Institute e.V. (FLI), Beutenbergstrasse 11, D-07745 Jena, Germany.
Stephan DiekmannLeibniz-Institute for Age Research - Fritz Lipmann Institute e.V. (FLI), Beutenbergstrasse 11, D-07745 Jena, Germany.
Leibniz Institute on Aging - Fritz Lipmann Institute (FLI) · DELeibniz Association · DELeibniz-Institut für Naturstoff-Forschung und Infektionsbiologie e. V. - Hans-Knöll-Institut (HKI) · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundRotenone inhibits the electron transfer from complex I to ubiquinone, in this way interfering with the electron transport chain in mitochondria. This chain of events induces increased levels of intracellular reactive oxygen species, which in turn can contribute to acceleration of telomere shortening and induction of DNA damage, ultimately resulting in aging. In this study, we investigated the effect of rotenone treatment in human fibroblast strains.

resultsFor the first time we here describe that rotenone treatment induced a hormetic effect in human fibroblast strains. We identified a number of genes which were commonly differentially regulated due to low dose rotenone treatment in fibroblasts independent of their cell origin. However, these genes were not among the most strongly differentially regulated genes in the fibroblast strains on treatment with rotenone. Thus, if there is a common hormesis regulation, it is superimposed by cell strain specific individual responses. We found the rotenone induced differential regulation of pathways common between the two fibroblast strains, being weaker than the pathways individually regulated in the single fibroblast cell strains. Furthermore, within the common pathways different genes were responsible for this different regulation. Thus, rotenone induced hormesis was related to a weak pathway signal, superimposed by a stronger individual cellular response, a situation as found for the differentially expressed genes.

conclusionWe found that the concept of hormesis also applies to in vitro aging of primary human fibroblasts. However, in depth analysis of the genes as well as the pathways differentially regulated due to rotenone treatment revealed cellular hormesis being related to weak signals which are superimposed by stronger individual cell-internal responses. This would explain that in general hormesis is a small effect. Our data indicate that the observed hormetic phenotype does not result from a specific strong well-defined gene or pathway regulation but from weak common cellular processes induced by low levels of reactive oxygen species. This conclusion also holds when comparing our results with those obtained for C. elegans in which the same low dose rotenone level induced a life span extending, thus hormetic effect.

Identifiers

PMID26380578
PMCPMC4572608
OpenAlexW1776705153

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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.