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Heat-Induced Pathophysiological and Metabolic Changes at the Feto-Maternal Interface Predisposing to Preterm Birth.

Isidore Mushimiyimana1, Lauren Richardson1, Thomas D Horvath2,3,4,5

  • 1Department of Obstetrics & Gynecology, Division of Basic Science and Translational Research, The University of Texas Medical Branch at Galveston, Galveston, Texas, USA.

FASEB Journal : Official Publication of the Federation of American Societies for Experimental Biology
|November 17, 2025
PubMed
Summary

Rising global temperatures and preterm birth (PTB) risk are linked. Heat stress harms maternal and fetal cells, causing mitochondrial dysfunction, oxidative stress, and inflammation, potentially contributing to PTB.

Keywords:
DNA damagefeto‐maternal interfaceinflammationmetabolismmitochondrial dysfunctionoxidative stresspreterm birthsenescence

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Area of Science:

  • Reproductive Biology
  • Environmental Health
  • Cellular Physiology

Background:

  • Global temperature rise is a growing concern linked to preterm birth (PTB).
  • Limited understanding of heat's pathophysiological mechanisms hinders clinical interventions for PTB.

Purpose of the Study:

  • To examine heat-induced pathophysiological and metabolic changes at feto-maternal interfaces (FMis).
  • To explore mechanistic implications of these changes in PTB pathophysiology.

Main Methods:

  • Utilized a 2D in vitro heat exposure model (39°C) with maternal decidual (DECs) and fetal amniotic epithelial cells (AECs).
  • Assessed mitochondrial function, oxidative stress (glutathione), stress signaling (p38MAPK, NF-κB), senescence, and inflammation (cytokines).
  • Employed targeted metabolomics to evaluate heat-induced metabolic shifts.

Main Results:

  • Heat stress induced mitochondrial dysfunction (reduced ATP, altered HSPD1, ATP5F1, VDAC1 expression) and oxidative stress (reduced GSH) in both cell types.
  • Heat exposure triggered DNA damage, p38MAPK activation, senescence, and increased inflammatory cytokines (IL-6, GM-CSF), indicating a senescence-associated secretory phenotype.
  • Metabolomic analysis revealed significant heat-induced shifts in energy, amino acid, epigenetic, and immune-related pathways, with both overlapping and cell-type-specific responses.

Conclusions:

  • Maternal and fetal cells are sensitive to heat stress, exhibiting differential pathobiologic and metabolic disruptions.
  • Findings provide insights into heat-induced cellular responses at the feto-maternal interface, contributing to PTB understanding.
  • Future models integrating multiple FMi cell types may identify heat-associated biomarkers for PTB prediction.