Premium
Redox modification of proteins as essential mediators of CNS autophagy and mitophagy
Author(s) -
Lizama-Manibusan Britney,
McLaughlin BethAnn
Publication year - 2013
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/j.febslet.2013.06.007
Subject(s) - mitophagy , autophagy , microbiology and biotechnology , reactive oxygen species , biology , signal transduction , oxidative stress , mitochondrion , programmed cell death , dna damage , cell signaling , parkin , neurodegeneration , parkinson's disease , biochemistry , dna , disease , apoptosis , medicine , pathology
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.