Evidence map›Paper›PMID 41255583›Full record

ArticleJuntendo medical journal2025

Molecular Mechanisms of Heatstroke: Pathophysiology and Cell Death Pathways.

Ricard Ferrer, Toshiaki Iba

Abstract read
In one paragraph

Article in Juntendo medical journal, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
–field-weighted citation impact
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

5 citing papers in PubMed.

  1. Review
  2. Review
  3. Review
  4. Sepsis and heatstroke: overlapping and distinct mechanisms of systemic inflammation.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2025
    Review
  5. Review
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.

Ricard Ferrer
Toshiaki Iba

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Heatstroke is a severe, life-threatening condition characterized by a core body temperature exceeding 40°C, accompanied by central nervous system dysfunction such as confusion, seizures, or coma. It often presents with systemic inflammation and multi-organ failure, including injury to the liver, kidneys, brain, and coagulation system. The molecular pathogenesis of heatstroke is multifactorial, involving a cascade of intracellular and extracellular events triggered by excessive heat. These include protein denaturation, loss of cellular homeostasis, oxidative stress, mitochondrial dysfunction, and the release of damage-associated molecular patterns (DAMPs) that activate immune responses. In parallel, regulated cell death pathways such as apoptosis, necroptosis, pyroptosis, and ferroptosis are initiated, amplifying tissue injury. Key molecular mediators include heat shock proteins, proinflammatory cytokines, and reactive oxygen species. This review summarizes current understanding of the molecular and cellular mechanisms underlying heatstroke, highlighting potential biomarkers and therapeutic targets that may improve diagnosis, prognostication, and clinical management of this increasingly relevant condition.

Indexed as

cell deathdamage-associated molecular patternsheat strokeleukocytemitochondria

Identifiers

PMID41255583
PMCPMC12620711

What OpenQuestion holds

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LicenceCC BY
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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.