Heat acclimation-mediated cross-tolerance in cardioprotection: Do HSP70 and HIF-1α play a role?

Michal Horowitz*, Halla Assadi

*Corresponding author for this work

Research output: Chapter in Book/Report/Conference proceedingConference contributionpeer-review

47 Scopus citations

Abstract

Heat acclimation (AC) is an evolutionarily conserved feature allowing adjustment to persistent changes in ambient temperature. The mechanisms underlying acclimation involve a continuum of physiologic changes, determined by temperature-adaptive shifts in gene expression. The AC heart generates greater pressure at lower O2 consumption, but at the expense of contractile velocity, and renders cytoprotection to a wide range of stressors (cross-tolerance) via greater cytoprotective protein reserves, faster post-injury molecular dynamic response, and post-translational modifications. A greater abundance of HSP70 and HIF-1α and its metabolic targeted genes (both nuclear and mitochondrial) are among the cytoprotective changes that occur. The cytoprotection profile provides a dual protective strategy - a constitutive availability of cytoprotective proteins without a need for de novo protein synthesis, together with an "alerted system" responding rapidly upon insult. Hence, cross-tolerance is achieved via activation of "on-call" constitutive cytoprotection shared by all stressors, together with organ-specific functional remodeling and stress-specific cross-talk.

Original languageEnglish
Title of host publicationAnalysis of Cardiac Development
Subtitle of host publicationFrom Embryo to Old Age
PublisherBlackwell Publishing Inc.
Pages199-206
Number of pages8
ISBN (Print)9781573317474
DOIs
StatePublished - Feb 2010

Publication series

NameAnnals of the New York Academy of Sciences
Volume1188
ISSN (Print)0077-8923
ISSN (Electronic)1749-6632

Keywords

  • Cross-tolerance
  • Heat-acclimation
  • HIF-1α
  • HSP70
  • Ischemicreperfusion insult
  • Stress-associated genes

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