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.
Original language | English (US) |
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Pages (from-to) | 52-59 |
Number of pages | 8 |
Journal | Neurobiology of Disease |
Volume | 43 |
Issue number | 1 |
DOIs | |
State | Published - Jul 2011 |
Funding
This study was supported by the National Institute of Neurologic Diseases and Stroke grant R01 NS38620 , and National Institute Child Health and Human Development grants T32 HD40686 and R01 HD045968 . We would also like to thank Henry Alexander and Christina Hosler for their expert technical assistance.
Keywords
- Autophagic stress
- Autophagosome
- Hypoxia-ischemia
- Lipophagy
- Mitophagy
- Traumatic brain injury
ASJC Scopus subject areas
- Neurology