TY - JOUR
T1 - Endoplasmic reticulum
T2 - ER stress regulates mitochondrial bioenergetics
AU - Bravo, Roberto
AU - Gutierrez, Tomás
AU - Paredes, Felipe
AU - Gatica, Damián
AU - Rodriguez, Andrea E.
AU - Pedrozo, Zully
AU - Chiong, Mario
AU - Parra, Valentina
AU - Quest, Andrew F G
AU - Rothermel, Beverly A.
AU - Lavandero, Sergio
N1 - Funding Information:
This research was funded in part by Comision Nacional de Ciencia y Tecnologia (CONICYT), Chile ( FONDECYT 1080436 to S.L.; FONDECYT 1110180 to M.C., FONDECYT 3110039 to Z.P.; FONDAP 15010006 to S.L., A.Q., and M.C.), the National Institutes of Health ( HL072016 , and HL097768 to B.A.R.) and the American Heart Association ( 0655202Y to B.A.R.). R.B., F.P., A.E.R. and V.P hold CONICYT PhD fellowships.
PY - 2012/1
Y1 - 2012/1
N2 - Endoplasmic reticulum (ER) stress activates an adaptive unfolded protein response (UPR) that facilitates cellular repair, however, under prolonged ER stress, the UPR can ultimately trigger apoptosis thereby terminating damaged cells. The molecular mechanisms responsible for execution of the cell death program are relatively well characterized, but the metabolic events taking place during the adaptive phase of ER stress remain largely undefined. Here we discuss emerging evidence regarding the metabolic changes that occur during the onset of ER stress and how ER influences mitochondrial function through mechanisms involving calcium transfer, thereby facilitating cellular adaptation. Finally, we highlight how dysregulation of ER-mitochondrial calcium homeostasis during prolonged ER stress is emerging as a novel mechanism implicated in the onset of metabolic disorders.
AB - Endoplasmic reticulum (ER) stress activates an adaptive unfolded protein response (UPR) that facilitates cellular repair, however, under prolonged ER stress, the UPR can ultimately trigger apoptosis thereby terminating damaged cells. The molecular mechanisms responsible for execution of the cell death program are relatively well characterized, but the metabolic events taking place during the adaptive phase of ER stress remain largely undefined. Here we discuss emerging evidence regarding the metabolic changes that occur during the onset of ER stress and how ER influences mitochondrial function through mechanisms involving calcium transfer, thereby facilitating cellular adaptation. Finally, we highlight how dysregulation of ER-mitochondrial calcium homeostasis during prolonged ER stress is emerging as a novel mechanism implicated in the onset of metabolic disorders.
KW - Calcium
KW - ER stress
KW - Endoplasmic reticulum-mitochondria axis
KW - Mitochondrial bioenergetics
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U2 - 10.1016/j.biocel.2011.10.012
DO - 10.1016/j.biocel.2011.10.012
M3 - Short survey
C2 - 22064245
AN - SCOPUS:83555176031
SN - 1357-2725
VL - 44
SP - 16
EP - 20
JO - International Journal of Biochemistry and Cell Biology
JF - International Journal of Biochemistry and Cell Biology
IS - 1
ER -