TY - GEN
T1 - Heat acclimation-mediated cross-tolerance in cardioprotection
T2 - Do HSP70 and HIF-1α play a role?
AU - Horowitz, Michal
AU - Assadi, Halla
PY - 2010/2
Y1 - 2010/2
N2 - 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.
AB - 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.
KW - Cross-tolerance
KW - Heat-acclimation
KW - HIF-1α
KW - HSP70
KW - Ischemicreperfusion insult
KW - Stress-associated genes
UR - http://www.scopus.com/inward/record.url?scp=77649127622&partnerID=8YFLogxK
U2 - 10.1111/j.1749-6632.2009.05101.x
DO - 10.1111/j.1749-6632.2009.05101.x
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AN - SCOPUS:77649127622
SN - 9781573317474
T3 - Annals of the New York Academy of Sciences
SP - 199
EP - 206
BT - Analysis of Cardiac Development
PB - Blackwell Publishing Inc.
ER -