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Related Concept Videos

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  3. Environment-induced Heat Stress Causes Ventricular-dependent Biochemical Changes In The Heart In Female Pigs.
  1. Home
  3. Environment-induced Heat Stress Causes Ventricular-dependent Biochemical Changes In The Heart In Female Pigs.

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Environment-induced heat stress causes ventricular-dependent biochemical changes in the heart in female pigs.

Melissa Roths1, Tori E Rudolph1, Alyssa D Freestone1

  • 1Department of Animal Science, Iowa State University, Ames, Iowa, USA.

Physiological Reports
|June 8, 2025

View abstract on PubMed

Summary
This summary is machine-generated.

Environment-induced heat stress (EIHS) causes ventricle-specific heart damage. The right ventricle shows increased protein breakdown, while the left ventricle exhibits altered calcium handling, potentially explaining previous findings of heart thickening.

Keywords:
heat strokeheatwavehyperthermiamuscleproteolysis

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Area of Science:

  • Cardiovascular Physiology
  • Environmental Health
  • Molecular Biology

Background:

  • Prolonged exposure to heat and humidity causes environment-induced heat stress (EIHS).
  • Previous research indicated EIHS induces ventricle-dependent cardiac changes.
  • The specific molecular mechanisms of EIHS-induced cardiac damage remain largely unelucidated.

Purpose of the Study:

  • To investigate the impact of EIHS on proteolysis and calcium homeostasis in the left ventricle (LV) and right ventricle (RV).
  • To test the hypothesis that EIHS increases proteolysis in the RV and causes calcium dysregulation in the LV.

Main Methods:

  • 3-month-old female pigs were exposed to thermoneutral (20°C) or EIHS (37.4°C) conditions for 24 hours.
  • Cardiac tissue from LV and RV was analyzed for markers of proteolysis and calcium regulatory proteins.
  • Quantitative analysis of protein abundance and activity was performed.

    • Main Results:

    • In the RV, EIHS increased markers of proteolysis, including calpain II, MuRF-1, MAFbx/Atrogin1, and calpain activity.
    • In the LV, EIHS elevated the abundance of calcium regulatory proteins such as PMCA, SERCA2a, STIM1, calsequestrin, CaMKII, and VDAC.
    • These findings reveal distinct ventricular responses to EIHS at the molecular level.

    Conclusions:

    • EIHS induces ventricle-specific alterations in cardiac molecular pathways.
    • The RV undergoes a shift towards proteolysis under EIHS conditions.
    • The LV experiences calcium dysregulation, potentially contributing to EIHS-induced ventricular thickening.