Autophagy in Neurotrauma: Good, Bad, or Dysregulated

Autophagy is a physiological process that helps maintain a balance between the manufacture of cellular components and breakdown of damaged organelles and other toxic cellular constituents. Changes in autophagic markers are readily detectable in the spinal cord and brain following neurotrauma, includ...

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Veröffentlicht in:Cells (Basel, Switzerland) Jg. 8; H. 7; S. 693
Hauptverfasser: Wu, Junfang, Lipinski, Marta M.
Format: Journal Article
Sprache:Englisch
Veröffentlicht: Switzerland MDPI AG 10.07.2019
MDPI
Schlagworte:
Animals
Apoptosis
autophagic flux
Autophagy
Autophagy - physiology
Biosynthesis
Brain - metabolism
Brain Injuries, Traumatic - metabolism
Brain Injuries, Traumatic - physiopathology
Cell cycle
Chemokines
Cytokines
Disease Models, Animal
Humans
Kinases
lysosomal damage
Lysosomes - metabolism
neuronal cell death
Neurons - metabolism
Neuroprotection
Organelles
Phagocytosis
Physiology
Proteins
Review
Spinal Cord - metabolism
Spinal cord injuries
Spinal Cord Injuries - metabolism
Spinal Cord Injuries - physiopathology
spinal cord injury
Trauma
Trauma, Nervous System - metabolism
Trauma, Nervous System - physiopathology
Traumatic brain injury
United States > US
autophagic flux
spinal cord injury
traumatic brain injury
neuronal cell death
autophagy
lysosomal damage
ISSN:2073-4409, 2073-4409
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Zusammenfassung:Autophagy is a physiological process that helps maintain a balance between the manufacture of cellular components and breakdown of damaged organelles and other toxic cellular constituents. Changes in autophagic markers are readily detectable in the spinal cord and brain following neurotrauma, including traumatic spinal cord and brain injury (SCI/TBI). However, the role of autophagy in neurotrauma remains less clear. Whether autophagy is good or bad is under debate, with strong support for both a beneficial and detrimental role for autophagy in experimental models of neurotrauma. Emerging data suggest that autophagic flux, a measure of autophagic degradation activity, is impaired in injured central nervous systems (CNS), and interventions that stimulate autophagic flux may provide neuroprotection in SCI/TBI models. Recent data demonstrating that neurotrauma can cause lysosomal membrane damage resulting in pathological autophagosome accumulation in the spinal cord and brain further supports the idea that the impairment of the autophagy–lysosome pathway may be a part of secondary injury processes of SCI/TBI. Here, we review experimental work on the complex and varied responses of autophagy in terms of both the beneficial and detrimental effects in SCI and TBI models. We also discuss the existing and developing therapeutic options aimed at reducing the disruption of autophagy to protect the CNS after injuries.
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ISSN:2073-4409
2073-4409
DOI:10.3390/cells8070693