Evidence map›Paper›PMID 38244765›Full record

ReviewCell stress & chaperones2024

Heat shock response during the resolution of inflammation and its progressive suppression in chronic-degenerative inflammatory diseases.

Helena Trevisan Schroeder, Carlos Henrique De Lemos Muller, Thiago Gomes Heck, Mauricio Krause, Paulo Ivo Homem de Bittencourt

Open access · goldAbstract readReview
In one paragraph

Review in Cell stress & chaperones, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
7.7field-weighted citation impact, top 2% 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

23 citing papers in PubMed, 33 citations in OpenAlex.

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  15. Identification of novel small molecule chaperone activators for neurodegenerative disease treatment.Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie · 2025
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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

5 authors at 2 institutions in 1 country.

Helena Trevisan SchroederLaboratory of Cellular Physiology (FisCel), Department of Physiology, Institute of Basic Health Sciences (ICBS), Federal University of Rio Grande do Sul (UFRGS), Porto Alegre, Rio Grande do Sul, Brazil.
Carlos Henrique De Lemos MullerLaboratory of Inflammation, Metabolism and Exercise Research (LAPIMEX), Department of Physiology, ICBS, UFRGS, Porto Alegre, Rio Grande do Sul, Brazil.
Thiago Gomes HeckPost Graduate Program in Integral Health Care (PPGAIS-UNIJUÍ/UNICRUZ/URI), Regional University of Northwestern Rio Grande Do Sul State (UNIJUI) and Post Graduate Program in Mathematical and Computational Modeling (PPGMMC), UNIJUI, Ijuí, Rio Grande do Sul, Brazil.
Mauricio KrauseLaboratory of Inflammation, Metabolism and Exercise Research (LAPIMEX), Department of Physiology, ICBS, UFRGS, Porto Alegre, Rio Grande do Sul, Brazil.
Paulo Ivo Homem de BittencourtLaboratory of Cellular Physiology (FisCel), Department of Physiology, Institute of Basic Health Sciences (ICBS), Federal University of Rio Grande do Sul (UFRGS), Porto Alegre, Rio Grande do Sul, Brazil. Electronic address: pauloivo@ufrgs.br.
Universidade Federal do Rio Grande do Sul · BRUniversidade Regional do Noroeste do Estado do Rio Grande do Sul · BR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The heat shock response (HSR) is a crucial biochemical pathway that orchestrates the resolution of inflammation, primarily under proteotoxic stress conditions. This process hinges on the upregulation of heat shock proteins (HSPs) and other chaperones, notably the 70 kDa family of heat shock proteins, under the command of the heat shock transcription factor-1. However, in the context of chronic degenerative disorders characterized by persistent low-grade inflammation (such as insulin resistance, obesity, type 2 diabetes, nonalcoholic fatty liver disease, and cardiovascular diseases) a gradual suppression of the HSR does occur. This work delves into the mechanisms behind this phenomenon. It explores how the Western diet and sedentary lifestyle, culminating in the endoplasmic reticulum stress within adipose tissue cells, trigger a cascade of events. This cascade includes the unfolded protein response and activation of the NOD-like receptor pyrin domain-containing protein-3 inflammasome, leading to the emergence of the senescence-associated secretory phenotype and the propagation of inflammation throughout the body. Notably, the activation of the NOD-like receptor pyrin domain-containing protein-3 inflammasome not only fuels inflammation but also sabotages the HSR by degrading human antigen R, a crucial mRNA-binding protein responsible for maintaining heat shock transcription factor-1 mRNA expression and stability on heat shock gene promoters. This paper underscores the imperative need to comprehend how chronic inflammation stifles the HSR and the clinical significance of evaluating the HSR using cost-effective and accessible tools. Such understanding is pivotal in the development of innovative strategies aimed at the prevention and treatment of these chronic inflammatory ailments, which continue to take a heavy toll on global health and well-being.

Indexed as

Diabetes Mellitus, Type 2Heat-Shock ProteinsHeat-Shock ResponseHeat Shock Transcription FactorsHSP70 Heat-Shock ProteinsHumansInflammasomesInflammationNLR ProteinsRNA, MessengerHeat-Shock ProteinsHeat Shock Transcription FactorsHSP70 Heat-Shock ProteinsInflammasomesNLR ProteinsRNA, MessengerChronic inflammatory diseasesExerciseHeat shock responseHSP70Insulin resistanceObesity

Identifiers

PMID38244765
PMCPMC10939074
OpenAlexW4391003955

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.