Cited by 29Genetics, Aging, and Longevity in Model OrganismsTelomeres, Telomerase, and SenescenceCell death mechanisms and regulation

Cell resilience in species life spans: a link to inflammation?

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Finch, Caleb E., Morgan, Todd E., Longo, Valter D., De Magalhaes, Joao P.·2010·Aging Cell

Abstract

Summary: Species differences in life span have been attributed to cellular survival during various stressors, designated here as ‘cell resilience’. In primary fibroblast cultures, cell resilience during exposure to free radicals, hypoglycemia, hyperthermia, and various toxins has shown generally consistent correlations with the species characteristic life spans of birds and mammals. However, the mechanistic links of cell resilience in fibroblast cultures to different species life spans are poorly understood. We propose that certain experimental stressors are relevant to somatic damage in vivo during inflammatory responses of innate immunity, particularly, resistance to reactive oxygen species (ROS), low glucose, and hyperthermia. According to this hypothesis, somatic cell resilience determines species differences in longevity during repeated infections and traumatic injuries in the natural environment. Infections and injury expose local fibroblasts and other cells to ROS generated by macrophages and to local temperature elevations. Systemically, acute phase immune reactions cause hypoglycemia and hyperthermia. We propose that cell resilience to somatic stressors incurred in inflammation is important in the evolution of longevity and that longer‐lived species are specifically more resistant to immune‐related stressors. This hypothesis further specifies Kirkwood’s disposable soma theory. We suggest expanding the battery of stressors and markers used for comparative studies to additional cell types and additional parameters relevant to host defense and to their ecological specificities.

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Crossref · 10.1111/j.1474-9726.2010.00578.x

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  • Inflammaging is a hallmark of nearly every major age-related disease and phenotype and a defining pathological feature of aging tissues across multiple species.

    “Inflammaging is a hallmark of virtually every major age-related disease and phenotype and has been shown to be a defining pathological characteristic of aging tissues across multiple species [5].”

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  1. Lacey EA Alexander RD Braude SH Sherman PW Jarvis JUM Sherman PW Jarvis JUM Alexander RD An ethogram for the naked mole-rat: nonvocal behaviors The Biology of the Mole-Rat 1991 209 242 Princeton University Press

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Authors
Finch, C. E., Morgan, T. E., Longo, V. D., & De Magalhaes, J. P.
Affiliations
University of Southern California (US)
Corresponding author
Finch, Caleb E.
Venue
Aging Cell
Publisher
Wiley
Published
2010-07-21
Volume
9
Issue
4
Pages
519-526
ISSN
  • 1474-9718 (ISSN-L)
  • 1474-9726
OpenAlex
W2098022090
Cited by
29
References
101
Citations by year
2025: 1 · 2024: 1 · 2023: 1 · 2022: 4 · 2020: 1 · 2019: 2 · 2018: 4 · 2017: 2 · 2016: 4 · 2015: 5 · 2014: 2 · 2012: 1
FWCI
0.22
Type
journal article
Language
en
Open access
Locations
  • Aging Cell (publishedVersion)
  • PubMed (publishedVersion)
  • PubMed Central (acceptedVersion)
Funders
  • Ellison Medical Foundation
  • Biotechnology and Biological Sciences Research Council (BB/G024774/1)
  • National Institute on Aging (AG026572, T32AG000093, AG20642, R01AG020642, AG025135, R01AG025135, P01AG026572)
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Aging › Genetics, Aging, and Longevity in Model Organisms
  • Health Sciences › Medicine › Physiology › Telomeres, Telomerase, and Senescence
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Cell death mechanisms and regulation
Keywords
inflammation, reactive oxygen species, hypoglycemia, hyperthermia, fibroblasts, disposable soma theory, innate immunity, macrophages, acute phase response, stress tolerance, comparative aging
MeSH terms
Acute-Phase Reaction, Animals, Cell Survival, DNA Damage, Fibroblasts, Immunity, Innate, Inflammation, Longevity, Models, Biological, Phylogeny, Species Specificity, Genome, Cell Death, Oxidative Stress

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