Endoplasmic reticulum: ER stress regulates mitochondrial bioenergetics

Roberto Bravo, Tomás Gutierrez, Felipe Paredes, Damián Gatica, Andrea E. Rodriguez, Zully Pedrozo, Mario Chiong, Valentina Parra, Andrew F G Quest, Beverly A. Rothermel, Sergio Lavandero

Research output: Contribution to journalShort survey

96 Scopus citations

Abstract

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.

Original languageEnglish (US)
Pages (from-to)16-20
Number of pages5
JournalInternational Journal of Biochemistry and Cell Biology
Volume44
Issue number1
DOIs
StatePublished - Jan 2012

Keywords

  • Calcium
  • ER stress
  • Endoplasmic reticulum-mitochondria axis
  • Mitochondrial bioenergetics

ASJC Scopus subject areas

  • Biochemistry
  • Cell Biology

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    Bravo, R., Gutierrez, T., Paredes, F., Gatica, D., Rodriguez, A. E., Pedrozo, Z., Chiong, M., Parra, V., Quest, A. F. G., Rothermel, B. A., & Lavandero, S. (2012). Endoplasmic reticulum: ER stress regulates mitochondrial bioenergetics. International Journal of Biochemistry and Cell Biology, 44(1), 16-20. https://doi.org/10.1016/j.biocel.2011.10.012