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Cited by 99Telomeres, Telomerase, and SenescenceMitochondrial Function and PathologyGenetics, Aging, and Longevity in Model Organisms

Sustained inhibition of oxidative phosphorylation impairs cell proliferation and induces premature senescence in human fibroblasts

Stöckl, Petra, Hütter, Eveline, Zwerschke, Werner, Jansen-Dürr, Pidder·2006·Experimental Gerontology
DOI 10.1016/j.exger.2006.04.009
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Abstract

The mitochondrial theory of aging predicts that functional alterations in mitochondria contribute to the aging process. Whereas this hypothesis implicates increased production of reactive oxygen species (ROS) as a driving force of the aging process, little is known about molecular mechanisms by which mitochondrial impairment might contribute to aging. Using cellular senescence as a model for human aging, we have recently reported partial uncoupling of the respiratory chain in senescent human fibroblasts. In the present communication, we address a potential cause-effect relationship between mitochondrial impairment and the appearance of a senescence-like phenotype in young cells. We found that treatment by antimycin A delays proliferation and induces premature senescence in a subset of the cells, associated with increased reactive oxygen species (ROS) production. Quenching of ROS by antioxidants did however not restore proliferation capacity nor prevent premature senescence. Premature senescence is also induced upon chronic exposure to oligomycin, irrespective of ROS production, and oligomycin treatment induced the up-regulation of the cdk inhibitors p16, p21 and p27, which are also up-regulated in replicative senescence. Thus, besides the well-established influence of ROS on proliferation and senescence, a reduction in the level of oxidative phosphorylation is causally related to reduced cell proliferation and the induction of premature senescence.

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  • It is possible to induce senescence in normal fibroblasts by using antimycin A or oligomycin.

    “This is consistent with other studies that found that it was possible to induce senescence in normal fibroblasts by using antimycin A or oligomycin (45).”

    From Mitochondrial Dysfunction Contributes to Oncogene-Induced Senescence (2009) · cites this paper as [45]

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Authors
Stöckl, P., Hütter, E., Zwerschke, W., & Jansen-Dürr, P.
Affiliations
Austrian Academy of Sciences (AT)
ORCID
Zwerschke, Werner
Venue
Experimental Gerontology
Publisher
Elsevier BV
Published
2006-07
Volume
41
Issue
7
Pages
674-682
ISSN
0531-5565 (ISSN-L)
DOI
10.1016/j.exger.2006.04.009
OpenAlex
W1973629945
Cited by
99
References
4
Citations by year
2026: 4 · 2025: 8 · 2024: 1 · 2023: 6 · 2022: 8 · 2021: 5 · 2020: 8 · 2019: 5 · 2018: 7 · 2017: 1 · 2016: 6 · 2015: 2 · 2014: 7 · 2013: 3 · 2012: 8
FWCI
2.65
Type
journal article
Language
en
Open access
closed
Licence
www.elsevier.com/tdm/userlicense/1.0/ (tdm)
Locations
  • Experimental Gerontology (publishedVersion)
  • PubMed (publishedVersion)
Topics
  • Health Sciences › Medicine › Physiology › Telomeres, Telomerase, and Senescence
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Aging › Genetics, Aging, and Longevity in Model Organisms
Keywords
oxidative phosphorylation, premature senescence, cellular senescence, human fibroblasts, antimycin A, oligomycin, reactive oxygen species, mitochondrial uncoupling, cell proliferation, cyclin-dependent kinase inhibitors, p16, p21, p27, replicative senescence, mitochondrial theory of aging, antioxidants
MeSH terms
Acetylcysteine, Adenosine Triphosphate, Cell Cycle, Cells, Cultured, Fibroblasts, Humans, Mitochondria, Oxidative Phosphorylation, Cellular Senescence, Reactive Oxygen Species, Cell Proliferation

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