Evidence map›Paper›PMID 27289378›Full record

ReviewCellular and molecular life sciences : CMLS2016

Metabolic control of the proteotoxic stress response: implications in diabetes mellitus and neurodegenerative disorders.

Kuo-Hui Su, Chengkai Dai

Open access · greenAbstract readReview
In one paragraph

Review in Cellular and molecular life sciences : CMLS, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.1field-weighted citation impact, top 24% 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

17 citing papers in PubMed, 20 citations in OpenAlex.

  1. Insulin Resistance and Inflammation.International journal of molecular sciences · 2026
    Review
  2. Article
  3. Review
  4. Review
  5. Review
  6. Review
  7. Article
  8. Article
  9. Article
  10. Review
  11. Review
  12. Tailoring of Proteostasis Networks with Heat Shock Factors.Cold Spring Harbor perspectives in biology · 2019
    Review
  13. Review
  14. Effect of BIS depletion on HSF1-dependent transcriptional activation in A549 non-small cell lung cancer cells.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2018
    Article
  15. Article
  16. Article
  17. Article
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

2 authors at 1 institution in 1 country.

Kuo-Hui SuThe Jackson Laboratory, 600 Main Street, Bar Harbor, ME, 04609, USA.
Chengkai DaiThe Jackson Laboratory, 600 Main Street, Bar Harbor, ME, 04609, USA. chengkai.dai@jax.org.ORCID 0000-0002-0726-3327
Jackson Laboratory · US

Funding

Shared Resource ManagementP30CA034196 · NCI · JACKSON LABORATORY · PI William Carl Skarnes · 1985 to 2026
$61.9M
Role of a Novel Stress Response Mechanism-Genetic Buffering-in Tumor EvolutionDP2OD007070 · OD · JACKSON LABORATORY · PI DAI, CHENGKAI · 2010 to 2010
$2.7M
(PQA1) Molecular Mechanism of Metformin in CancerR21CA184704 · NCI · JACKSON LABORATORY · PI DAI, CHENGKAI · 2014 to 2015
$419k
NCI NIH HHS P30 CA034196NCI NIH HHS R21 CA184704NIH HHS DP2 OD007070
6 · The paper itself

Abstract

Proteome homeostasis, or proteostasis, is essential to maintain cellular fitness and its disturbance is associated with a broad range of human health conditions and diseases. Cells are constantly challenged by various extrinsic and intrinsic insults, which perturb cellular proteostasis and provoke proteotoxic stress. To counter proteomic perturbations and preserve proteostasis, cells mobilize the proteotoxic stress response (PSR), an evolutionarily conserved transcriptional program mediated by heat shock factor 1 (HSF1). The HSF1-mediated PSR guards the proteome against misfolding and aggregation. In addition to proteotoxic stress, emerging studies reveal that this proteostatic mechanism also responds to cellular energy state. This regulation is mediated by the key cellular metabolic sensor AMP-activated protein kinase (AMPK). In this review, we present an overview of the maintenance of proteostasis by HSF1, the metabolic regulation of the PSR, particularly focusing on AMPK, and their implications in the two major age-related diseases-diabetes mellitus and neurodegenerative disorders.

Indexed as

AnimalsDiabetes MellitusHeat-Shock ProteinsHumansModels, BiologicalNeurodegenerative DiseasesProteinsStress, PhysiologicalHeat-Shock ProteinsProteinsAlzheimer’s diseaseDementiaHeat shock responseInsulin resistanceMetabolic stressMetforminMolecular chaperone/HSPPolyQ diseases

Identifiers

PMID27289378
PMCPMC5599143
OpenAlexW2415251165

What OpenQuestion holds

Textmetadata
LicenceTDM
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.