Evidence map›Paper›PMID 29203714›Full record

ReviewPhilosophical transactions of the Royal Society of London. Series B, Biological sciences2018

Exercise, heat shock proteins and insulin resistance.

Ashley E Archer, Alex T Von Schulze, Paige C Geiger

Open access · bronzeAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Philosophical transactions of the Royal Society of London. Series B, Biological sciences, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 71 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
71citing papers in PubMed, 3 pooled it
3.2field-weighted citation impact, top 7% 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

71 citing papers in PubMed, 3 syntheses or guidelines pooled it, 121 citations in OpenAlex.

  1. Pooled it
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  4. Trial
  5. Review
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  7. Article
  8. Insulin Resistance and Inflammation.International journal of molecular sciences · 2026
    Review
  9. Diabetes, Protein Misfolding, and Heat Stress: Molecular Insights and Translational Perspectives.TH open : companion journal to thrombosis and haemostasis · 2026
    Review
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11 more citing papers are in PubMed but not listed here.

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

3 authors at 1 institution in 1 country.

Ashley E ArcherDepartment of Molecular and Integrative Physiology, University of Kansas Medical Center, Kansas City, KS, USA.
Alex T Von SchulzeDepartment of Molecular and Integrative Physiology, University of Kansas Medical Center, Kansas City, KS, USA.
Paige C GeigerDepartment of Molecular and Integrative Physiology, University of Kansas Medical Center, Kansas City, KS, USA pgeiger@kumc.edu.ORCID http://orcid.org/0000-0002-3990-7246
Google (United States) · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Best known as chaperones, heat shock proteins (HSPs) also have roles in cell signalling and regulation of metabolism. Rodent studies demonstrate that heat treatment, transgenic overexpression and pharmacological induction of HSP72 prevent high-fat diet-induced glucose intolerance and skeletal muscle insulin resistance. Overexpression of skeletal muscle HSP72 in mice has been shown to increase endurance running capacity nearly twofold and increase mitochondrial content by 50%. A positive correlation between HSP72 mRNA expression and mitochondrial enzyme activity has been observed in human skeletal muscle, and HSP72 expression is markedly decreased in skeletal muscle of insulin resistant and type 2 diabetic patients. In addition, decreased levels of HSP72 correlate with insulin resistance and non-alcoholic fatty liver disease progression in livers from obese patients. These data suggest the targeted induction of HSPs could be a therapeutic approach for preventing metabolic disease by maintaining the body's natural stress response. Exercise elicits a number of metabolic adaptations and is a powerful tool in the prevention and treatment of insulin resistance. Exercise training is also a stimulus for increased HSP expression. Although the underlying mechanism(s) for exercise-induced HSP expression are currently unknown, the HSP response may be critical for the beneficial metabolic effects of exercise. Exercise-induced extracellular HSP release may also contribute to metabolic homeostasis by actively restoring HSP72 content in insulin resistant tissues containing low endogenous levels of HSPs.This article is part of the theme issue 'Heat shock proteins as modulators and therapeutic targets of chronic disease: an integrated perspective'.

Indexed as

AnimalsExerciseHeat-Shock ProteinsHumansInsulin ResistanceMicePhysical Conditioning, AnimalRatsHeat-Shock Proteinsaerobic capacityheat treatmentinflammationmitochondriaskeletal muscle

Identifiers

PMID29203714
PMCPMC5717529
OpenAlexW2772015960

What OpenQuestion holds

Textmetadata
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.