title: Endoplasmic reticulum: ER stress regulates mitochondrial bioenergetics.
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.
authors: Centro Estudios Moleculares de la Celula, Facultad Ciencias Quimicas y Farmaceuticas, Universidad de Chile, Santiago, Chile.
authors: Roberto
authors: R
authors: Bravo
authors: Tomás
authors: T
authors: Gutierrez
authors: Felipe
authors: F
authors: Paredes
authors: Damián
authors: D
authors: Gatica
authors: Andrea E
authors: AE
authors: Rodriguez
authors: Zully
authors: Z
authors: Pedrozo
authors: Mario
authors: M
authors: Chiong
authors: Valentina
authors: V
authors: Parra
authors: Andrew F G
authors: AF
authors: Quest
authors: Beverly A
authors: BA
authors: Rothermel
authors: Sergio
authors: S
authors: Lavandero
mesh_terms: D004721:Endoplasmic Reticulum / Q000378:metabolism / Q000502:physiology*; D059865:Endoplasmic Reticulum Stress / Q000502:physiology*; D004734:Energy Metabolism; D006801:Humans; D008928:Mitochondria / Q000378:metabolism / Q000502:physiology*