TY - JOUR
T1 - Heat acclimation mediated cardioprotection is controlled by mitochondrial metabolic remodeling involving HIF-1α
AU - Mreisat, A.
AU - Kanaani, H.
AU - Saada, A.
AU - Horowitz, M.
N1 - Publisher Copyright:
© 2020 Elsevier Ltd
PY - 2020/10
Y1 - 2020/10
N2 - 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.
AB - 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.
KW - Cardiomyocyte rigor contracture
KW - Heat acclimation mediated cross-tolerance
KW - HIF-1α targets
KW - LDHb (mitochondrial)
KW - Oxygen consumption
KW - Pyruvate utilization
KW - ROS
UR - http://www.scopus.com/inward/record.url?scp=85090559858&partnerID=8YFLogxK
U2 - 10.1016/j.jtherbio.2020.102691
DO - 10.1016/j.jtherbio.2020.102691
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C2 - 33077115
AN - SCOPUS:85090559858
SN - 0306-4565
VL - 93
JO - Journal of Thermal Biology
JF - Journal of Thermal Biology
M1 - 102691
ER -