ArticleCell stress & chaperones2008
Recovery from stress is a function of age and telomere length.
Article in Cell stress & chaperones, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
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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
6 citing papers in PubMed, 7 citations in OpenAlex.
- Relationship Between Occupational Characteristics and Telomere Length in Female Nurses Aged 20-39 Years: A Cross-Sectional Study.Healthcare (Basel, Switzerland) · 2026Article
- Effects of Thyme (Antioxidants (Basel, Switzerland) · 2023Article
- Observational
- The importance of the cellular stress response in the pathogenesis and treatment of type 2 diabetes.Cell stress & chaperones · 2014Article
- Sublethal heat shock induces premature senescence rather than apoptosis in human mesenchymal stem cells.Cell stress & chaperones · 2014Article
- Potential epigenetic mechanism(s) associated with the persistence of psychoneurological symptoms in women receiving chemotherapy for breast cancer: a hypothesis.Biological research for nursing · 2014Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cells are constantly exposed to a wide variety of stimuli and must be able to mount appropriate physiological responses in order to maintain proper form and function. Cells from every organism have evolved highly conserved mechanisms to cope with environmental changes, including the widely studied heat shock response (HSR), which is induced by a variety of cellular stresses such as heavy metal ion exposure. It has long been known that as organisms and individual cells age, their ability to appropriately cope with environmental stress is attenuated. Here, we examine the ability of two heavy metal ions (ZnCl(2), SnCl(2)) to induce the HSR in human fibroblasts by assessing the expression of heat shock proteins (Hsp90, Hsp70, and p23) and the ability of the cells to recover over time. We demonstrate that the induction and recovery of chaperone levels is attenuated with age and that cells immortalized with the human telomerase reverse transcriptase component of the telomerase enzyme do not attenuate their HSR as their replicative age increases. Our data suggest that the recovery of normal human cells from an HSR is related in part to age and the cell's overall telomere length.
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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.