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Exercise mitigates reductive stress-induced cardiac remodeling in mice.

Arun Jyothidasan1, Sini Sunny1, Asokan Devarajan2

  • 1Cardiac Aging & Redox Signaling Laboratory, Molecular and Cellular Pathology, Department of Pathology/Center for Free Radical Biology, University of Alabama at Birmingham, Birmingham, AL, USA.

Redox Biology
|July 25, 2024
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Summary

Prolonged treadmill exercise mitigated endoplasmic reticulum (ER) dysfunction and cardiac remodeling in mice with constitutive Nrf2 activation. Exercise improved ER-associated degradation (ERAD) function and autophagy flux, highlighting its protective role against reductive stress-associated pathology.

Keywords:
Cardiac hypertrophyER stressExerciseNrf2 signalingOxidative stressProteostasisReductive stress

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Area of Science:

  • Cardiovascular Biology
  • Cellular Proteostasis
  • Exercise Physiology

Background:

  • The endoplasmic reticulum (ER) is crucial for protein folding and cellular proteostasis.
  • Chronic reductive stress (RS) impairs ER function in cardiomyocytes.
  • Constitutive Nrf2 activation in cardiac-specific Nrf2 transgenic (CaNrf2-TG) mice exacerbates ER transcriptome alterations and protein aggregation.

Purpose of the Study:

  • To investigate if prolonged moderate treadmill exercise can mitigate RS-induced ER dysfunction and cardiac remodeling in CaNrf2-TG mice.
  • To elucidate the effects of exercise on ER transcriptome, protein folding, ER-associated degradation (ERAD), and autophagy.
  • To assess the prophylactic potential of exercise in maintaining cardiac function under chronic RS.

Main Methods:

  • Utilized RNA sequencing to analyze ER transcriptome alterations in CaNrf2-TG hearts at various ages.
  • Quantified ubiquitinated proteins and VCP levels as markers of ERAD function.
  • Implemented a 20-week treadmill exercise intervention starting at 6 weeks of age.
  • Assessed cardiomyocyte hypertrophy, cardiac function, antioxidant levels, ER stress markers, ERAD function, and autophagy flux (LC-I to LC-II).

Main Results:

  • CaNrf2-TG hearts showed significant downregulation of ER genes and increased ubiquitinated proteins over time, indicating impaired protein folding and augmented ERAD.
  • Exercise intervention reduced cardiomyocyte hypertrophy and preserved cardiac function in TG mice.
  • Exercise did not alter antioxidant or ER stress protein levels but significantly improved ERAD function and autophagy flux in TG-EXE hearts.

Conclusions:

  • Constitutive Nrf2 activation combined with RS leads to ER dysfunction and cardiac pathology.
  • Exercise demonstrates prophylactic potential against RS-associated cardiac pathology.
  • Exercise mitigates cardiac remodeling and preserves function, potentially through ER-independent mechanisms enhancing ERAD and autophagy.