title: Autophagy in acute brain injury: feast, famine, or folly?
abstract: In the central nervous system, increased autophagy has now been reported after traumatic brain and spinal cord injury, cerebral ischemia, intracerebral hemorrhage, and seizures. This increase in autophagy could be physiologic, converting damaged or dysfunctional proteins, lipids, and/or organelles to their amino acid and fatty acid components for recycling. On the other hand, this increase in autophagy could be supraphysiologic, perhaps consuming and eliminating functional proteins, lipids, and/or organelles as well. Whether an increase in autophagy is beneficial (feast) or detrimental (famine) in brain likely depends on both the burden of intracellular substrate targeted for autophagy and the capacity of the cell's autophagic machinery. Of course, increased autophagy observed after brain injury could also simply be an epiphenomenon (folly). These divergent possibilities have clear ramifications for designing therapeutic strategies targeting autophagy after acute brain injury and are the subject of this review. This article is part of a Special Issue entitled "Autophagy and protein degradation in neurological diseases."
authors.affiliation: Department of Critical Care Medicine, Safar Center for Resuscitation Research, Brain Trauma Research Center, and Children's Hospital of Pittsburgh of UPMC, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania 15260, USA.
authors.forename: Craig M
authors.initials: CM
authors.lastname: Smith
authors.forename: Yaming
authors.initials: Y
authors.lastname: Chen
authors.forename: Mara L
authors.initials: ML
authors.lastname: Sullivan
authors.forename: Patrick M
authors.initials: PM
authors.lastname: Kochanek
authors.forename: Robert S B
authors.initials: RS
authors.lastname: Clark
mesh_terms: D000818:Animals; D001343:Autophagy / Q000502:physiology*; D001930:Brain Injuries / Q000473:pathology* / Q000503:physiopathology / Q000628:therapy; D006706:Homeostasis / Q000502:physiology; D006801:Humans; D020925:Hypoxia-Ischemia, Brain / Q000473:pathology / Q000503:physiopathology / Q000628:therapy