BethAnn McLaughlin
Faculty Member
Last active: 4/25/2016

Redox modification of proteins as essential mediators of CNS autophagy and mitophagy.

Lizama-Manibusan B, McLaughlin B
FEBS Lett. 2013 587 (15): 2291-8

PMID: 23773928 · PMCID: PMC5125300 · DOI:10.1016/j.febslet.2013.06.007

Production of cellular reactive oxygen species (ROS) is typically associated with protein and DNA damage, toxicity, and death. However, ROS are also essential regulators of signaling and work in concert with redox-sensitive proteins to regulate cell homeostasis during stress. In this review, we focus on the redox regulation of mitophagy, a process that contributes to energetic tone as well as mitochondrial form and function. Mitophagy has been increasingly implicated in diseases including Parkinson's, Amyotrophic Lateral Sclerosis, and cancer. Although these disease states employ different genetic mutations, they share the common factors of redox dysregulation and autophagic signaling. This review highlights key redox sensitive signaling molecules which can enhance neuronal survival by promoting temporally and spatially controlled autophagic signaling and mitophagy.

Copyright © 2013 Federation of European Biochemical Societies. Published by Elsevier B.V. All rights reserved.

MeSH Terms (9)

Animals Autophagy Central Nervous System Humans Mitochondrial Degradation Oxidation-Reduction Proteins Reactive Oxygen Species Signal Transduction

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