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Responses to Heat and Cold Stress02:45

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Every organism has an optimum temperature range within which healthy growth and physiological functioning can occur. At the ends of this range, there will be a minimum and maximum temperature that interrupt biological processes.
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Updated: Apr 23, 2026

A Preclinical Model of Exertional Heat Stroke in Mice
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Temperature-Gradient Transcriptomic Atlas Reveals the PPAR Signaling Pathway Dysfunction in Heat Stroke Induced Liver

Ying Zhu1,2, Wanlin Liu2, Chunyuan Yang2

  • 1School of Basic Medical Sciences Anhui Medical University Hefei China.

FASEB Bioadvances
|April 22, 2026
PubMed
Summary
This summary is machine-generated.

Heat stroke causes severe liver injury through metabolic reprogramming, particularly affecting lipid metabolism via the PPAR signaling pathway. This study identifies key molecular changes and potential therapeutic targets for heat stroke interventions.

Keywords:
PPAR signaling pathwayheat strokelipid metabolic reprogrammingliver injuryprogressive metabolic dysfunction

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Area of Science:

  • Physiology
  • Molecular Biology
  • Toxicology

Background:

  • Heat stroke (HS) is a severe hyperthermia with high mortality, frequently causing liver injury and multi-organ failure.
  • The molecular mechanisms of HS-induced liver damage are not fully understood, necessitating further research, especially with increasing global extreme heat events.

Purpose of the Study:

  • To investigate the molecular mechanisms of liver injury during heat stroke using a stepwise murine model.
  • To identify temperature-dependent molecular changes and pathways involved in heat stroke-induced hepatic damage.

Main Methods:

  • Established a graded murine heat stroke model by gradually increasing core body temperature from 40°C to 43°C.
  • Performed hematological, biochemical, and histopathological analyses on collected blood and liver tissues.
  • Conducted transcriptomic profiling of murine livers to identify differentially expressed genes (DEGs) and enriched pathways.
  • Validated key DEGs and protein expression using RT-qPCR and immunohistochemistry.

Main Results:

  • Significant liver injury, characterized by elevated ALT/AST, weight loss, and histopathological changes, was observed at core temperatures ≥42°C.
  • Transcriptomic analysis revealed temperature-dependent DEGs involved in inflammation, lipid metabolism, apoptosis, and stress responses from 41°C onwards.
  • The peroxisome proliferator-activated receptor (PPAR) signaling pathway was identified as significantly enriched and dysregulated, indicating temperature-dependent metabolic reprogramming, particularly in lipid metabolism.
  • Protein validation confirmed the transcriptomic findings, highlighting CD36, ACOX3, and PPARα responses to heat stress.

Conclusions:

  • Heat stroke-induced liver injury is linked to progressive metabolic reprogramming, with disrupted lipid metabolism playing a central pathogenic role.
  • Dysregulated PPAR signaling is a key temperature-dependent feature of liver injury during heat stroke, suggesting its potential as a therapeutic target.
  • This study provides a temporal framework and molecular candidates for developing mechanism-directed interventions for heat stroke.