Reductive stress impairs myoblasts mitochondrial function and triggers mitochondrial hormesis

Even though oxidative stress damage from excessive production of ROS is a well known phenomenon, the impact of reductive stress remains poorly understood. This study tested the hypothesis that cellular reductive stress could lead to mitochondrial malfunction, triggering a mitochondrial hormesis (mit...

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Bibliographic Details
Published in:	Biochimica et biophysica acta Vol. 1853; no. 7; pp. 1574 - 1585
Main Authors:	Singh, François, Charles, Anne-Laure, Schlagowski, Anna-Isabel, Bouitbir, Jamal, Bonifacio, Annalisa, Piquard, François, Krähenbühl, Stephan, Geny, Bernard, Zoll, Joffrey
Format:	Journal Article
Language:	English
Published:	Netherlands Elsevier B.V 01.07.2015
Subjects:	Acetylcysteine - pharmacology Animals Apoptosis Cell Respiration - drug effects Cell Survival - drug effects Cytoprotection - drug effects Hormesis - drug effects Hydroxymethylglutaryl-CoA Reductase Inhibitors - pharmacology Mitochondria - drug effects Mitochondria - metabolism Mitochondrial Turnover - drug effects Mitohormesis Myoblast Myoblasts - drug effects Myoblasts - metabolism N-acetylcysteine Oxidation-Reduction - drug effects Protective Agents - pharmacology Rats Reactive Oxygen Species - metabolism Reductive stress Statin Stress, Physiological - drug effects Time Factors Myoblast Reductive stress Statin Mitohormesis N-acetylcysteine Apoptosis
ISSN:	0167-4889, 0006-3002, 1879-2596
Online Access:	Get full text
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