title: Redox modification of proteins as essential mediators of CNS autophagy and mitophagy.
abstract: 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.
authors.affiliation: Vanderbilt Brain Institute, Vanderbilt University School of Medicine, Nashville, TN 37221, USA.
authors.forename: Britney
authors.initials: B
authors.lastname: Lizama-Manibusan
authors.forename: Bethann
authors.initials: B
authors.lastname: McLaughlin
mesh_terms: D000818:Animals; D001343:Autophagy; D002490:Central Nervous System / Q000276:immunology / Q000378:metabolism*; D006801:Humans; D063306:Mitophagy; D010084:Oxidation-Reduction; D011506:Proteins / Q000378:metabolism*; D017382:Reactive Oxygen Species / Q000378:metabolism; D015398:Signal Transduction
chemical_list: D011506:Proteins; D017382:Reactive Oxygen Species
keywords: Amyotrophic lateral sclerosis; Atg; Energetics; FOXO; HIF; Isocitrate dehydrogenase; Mitochondria; Mitophagy; Neurodegeneration; Parkinson’s disease; Reactive oxygen species; Sirtuin; p66shc