Mitochondrial stress management: a dynamic journey
Authors:Miriam Valera-Alberni1,2 and Carles Canto1
1 Nestlé Institute of Health Sciences (NIHS), EPFL Innovation Park, 1015 Lausanne.
2 School of Life Sciences, EPFL, 1015 Lausanne.
Keywords:
mitochondria, mitochondrial dynamics, oxidative stress, unfolded protein response, mitophagy, mitochondrial biogenesis.
Abbreviations:
α-KG – α-ketoglutarate,
Aβ – amyloid β peptide,
AMPK – AMP-activated protein kinase,
AP – autophagosome,
CAT – catalase,
CHOP – C/EBP homologous protein,
CLPP - ATP-dependent caseinolytic protease proteolytic subunit,
COX - cytochrome C oxidase,
ER – endoplasmic reticulum,
GPx – glutathione peroxidases,
IMM – inner mitochondrial membrane,
IMS – intermembrane space,
ISR – integrated stress response,
MDP – mitochondrial derived peptide,
MSR – mitochondrial stress response,
mtDNA – mitochondria DNA,
OMM – outer mitochondrial membrane,
OXPHOS – oxidative phosphorylation,
PERK – protein kinase RNA-like ER kinase,
PGC-1α – Peroxisome Proliferator Activator Receptor Gamma Coactivator 1a,
PINK1 – PTEN-induced putative kinase 1,
ROS – reactive oxygen species,
SOD – superoxide dismutase,
TCA – tricarboxylic acid cycle,
TrRx – Thioredoxin reductases,
UPR – unfolded protein response,
ΔΨm – mitochondrial membrane potential.
Corresponding Author(s):
Conflict of interest statement:
MV‐A and CC are employees of the Nestlé Institute of Health Sciences S.A.
Please cite this article as:
Miriam Valera-Alberni and Carles Canto (2018). Mitochondrial stress management: a dynamic journey. Cell Stress 2(10): 253-274. doi: 10.15698/cst2018.10.158
© 2018 Valera-Alberni and Canto. This is an open-access article released under the terms of the Creative Commons Attribution (CC BY) license, which allows the unrestricted use, distribution, and reproduction in any medium, provided the original author and source are acknowledged.
Abstract:
Mitochondria undergo continuous challenges in the course of their life, from their generation to their degradation. These challenges include the management of reactive oxygen species, the proper assembly of mitochondrial respiratory complexes and the need to balance potential mutations in the mitochondrial DNA. The detection of damage and the ability to keep it under control is critical to fine-tune mitochondrial function to the organismal energy needs. In this review, we will analyze the multiple mechanisms that safeguard mitochondrial function in light of in crescendo damage. This sequence of events will include initial defense against excessive reactive oxygen species production, compensation mechanisms by the unfolded protein response (UPRmt), mitochondrial dynamics and elimination by mitophagy.