Heat acclimation mediated cardioprotection is controlled by mitochondrial metabolic remodeling involving HIF-1α

A. Mreisat, H. Kanaani, A. Saada*, M. Horowitz*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

8 Scopus citations

Abstract

Heat acclimation (HA) induces metabolic plasticity to resist the effects of environmental heat with cross-tolerance to novel stressors such as oxygen supply perturbations, exercise, and alike. Our previous results indicated that hypoxia inducible transcription factor (HIF-1α) contributes to this adaptive process. In the present study, we link functional studies in isolated cardiomyocytes, with molecular and biochemical studies of cardiac mitochondria and demonstrate that HA remodels mitochondrial metabolism and performance. We observed the significant role that HIF-1α plays in the HA heart, as HA reduces oxidative stress during ischemia by shifting mitochondrial substrate preference towards pyruvate, with elevated level and activity of mitochondrial LDH (LDHb), acting a pivotal role. Increased antioxidative capacity to encounter hazards is implicated. These results deepen our understanding of heat acclimation-mediated cross tolerance (HACT), in which adaptive bioenergetic-mechanisms counteract the hazards of oxidative stress.

Original languageEnglish
Article number102691
JournalJournal of Thermal Biology
Volume93
DOIs
StatePublished - Oct 2020

Bibliographical note

Publisher Copyright:
© 2020 Elsevier Ltd

Keywords

  • Cardiomyocyte rigor contracture
  • Heat acclimation mediated cross-tolerance
  • HIF-1α targets
  • LDHb (mitochondrial)
  • Oxygen consumption
  • Pyruvate utilization
  • ROS

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