Evidence map›Paper›PMID 38059913›Full record

ArticleeLife2023

Hsf1 and the molecular chaperone Hsp90 support a 'rewiring stress response' leading to an adaptive cell size increase in chronic stress.

Samarpan Maiti, Kaushik Bhattacharya, Diana Wider, Dina Hany, Olesya Panasenko, Lilia Bernasconi, Nicolas Hulo, Didier Picard

Erratum issuedOpen access · goldAbstract read
In one paragraph

Article in eLife, 2023. 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 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
3.2field-weighted citation impact, top 8% 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

16 citing papers in PubMed, 21 citations in OpenAlex.

  1. Adaptation to heat stress by diversification of the vertebrate heat shock transcription factor family.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2026
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  4. Science advances · 2026
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  16. HSP90 multi-functionality in cancer.Frontiers in immunology · 2024
    Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

8 authors at 1 institution in 2 countries.

Samarpan MaitiDépartement de Biologie Moléculaire et Cellulaire, Université de Genève, Genève, Switzerland.ORCID 0000-0001-9090-2398
Kaushik BhattacharyaDépartement de Biologie Moléculaire et Cellulaire, Université de Genève, Genève, Switzerland.
Diana WiderDépartement de Biologie Moléculaire et Cellulaire, Université de Genève, Genève, Switzerland.
Dina HanyDépartement de Biologie Moléculaire et Cellulaire, Université de Genève, Genève, Switzerland.
Olesya PanasenkoBioCode: RNA to Proteins Core Facility, Département de Microbiologie et Médecine Moléculaire, Faculté de Médecine, Université de Genève, Genève, Switzerland.
Lilia BernasconiDépartement de Biologie Moléculaire et Cellulaire, Université de Genève, Genève, Switzerland.
Nicolas HuloInstitute of Genetics and Genomics of Geneva, Université de Genève, Genève, Switzerland.ORCID 0000-0003-2640-636X
Didier PicardDépartement de Biologie Moléculaire et Cellulaire, Université de Genève, Genève, Switzerland.ORCID 0000-0001-8816-9668
University of Geneva · CH

Funding

Schweizerischer Nationalfonds zur Förderung der Wissenschaftlichen Forschung 31003A_172789/1
6 · The paper itself

Abstract

Cells are exposed to a wide variety of internal and external stresses. Although many studies have focused on cellular responses to acute and severe stresses, little is known about how cellular systems adapt to sublethal chronic stresses. Using mammalian cells in culture, we discovered that they adapt to chronic mild stresses of up to two weeks, notably proteotoxic stresses such as heat, by increasing their size and translation, thereby scaling the amount of total protein. These adaptations render them more resilient to persistent and subsequent stresses. We demonstrate that Hsf1, well known for its role in acute stress responses, is required for the cell size increase, and that the molecular chaperone Hsp90 is essential for coupling the cell size increase to augmented translation. We term this translational reprogramming the 'rewiring stress response', and propose that this protective process of chronic stress adaptation contributes to the increase in size as cells get older, and that its failure promotes aging.

Indexed as

DNA-Binding ProteinsTranscription FactorsAnimalsHeat Shock Transcription FactorsHSP90 Heat-Shock ProteinsMammalsMolecular ChaperonesDNA-Binding ProteinsHeat Shock Transcription FactorsHSP90 Heat-Shock ProteinsMolecular ChaperonesTranscription Factorsagingcell biologycytoplasmic densityhumanproteostasissenescencestress adaptationtranslation

Identifiers

PMID38059913
PMCPMC10703448
OpenAlexW4379162400

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

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.