2019
DOI: 10.3390/cells8070693
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Autophagy in Neurotrauma: Good, Bad, or Dysregulated

Abstract: 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… Show more

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Cited by 96 publications
(69 citation statements)
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References 175 publications
(274 reference statements)
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“…Autophagy, an additional process, accelerates the destruction of cells via self-digestion, and is involved in type II (autophagic) cell death, which is distinguishable from type I (apoptotic) cell death ( Shintani and Klionsky, 2004 ). We hence quantified both transcriptional and translational expression levels of p62 and protein expression of LC3-II, two classical autophagy markers known to change in human and animal TBI studies ( Wu and Lipinski, 2019 ). Declines in p62 and elevations in LC3-II/LC3-I ratio were evident at 24 hr following TBI, and are associated with an enhancement of autophagy initiation in accord with prior CCI TBI studies ( Wu and Lipinski, 2019 ; Zeng et al, 2018 ).…”
Section: Discussionmentioning
confidence: 99%
See 1 more Smart Citation
“…Autophagy, an additional process, accelerates the destruction of cells via self-digestion, and is involved in type II (autophagic) cell death, which is distinguishable from type I (apoptotic) cell death ( Shintani and Klionsky, 2004 ). We hence quantified both transcriptional and translational expression levels of p62 and protein expression of LC3-II, two classical autophagy markers known to change in human and animal TBI studies ( Wu and Lipinski, 2019 ). Declines in p62 and elevations in LC3-II/LC3-I ratio were evident at 24 hr following TBI, and are associated with an enhancement of autophagy initiation in accord with prior CCI TBI studies ( Wu and Lipinski, 2019 ; Zeng et al, 2018 ).…”
Section: Discussionmentioning
confidence: 99%
“…We hence quantified both transcriptional and translational expression levels of p62 and protein expression of LC3-II, two classical autophagy markers known to change in human and animal TBI studies ( Wu and Lipinski, 2019 ). Declines in p62 and elevations in LC3-II/LC3-I ratio were evident at 24 hr following TBI, and are associated with an enhancement of autophagy initiation in accord with prior CCI TBI studies ( Wu and Lipinski, 2019 ; Zeng et al, 2018 ). DP treatment, in particular, normalized levels of both p62 and LC3-II, and thereby lowered TBI-induced autophagy, of potential importance as both excessive as well as too little autophagy appear to contribute to cell death ( Gómez-Díaz and Ikeda, 2019 ; Nopparat et al, 2010 ).…”
Section: Discussionmentioning
confidence: 99%
“…Neuron dysfunction induced by TBI is derived from primary and secondary brain injury mechanisms, and secondary injury results from delayed neurochemical, metabolic, and cellular changes (Feng et al, 2017). Further, disruption of autophagy flux is one of the mechanical attributes to secondary injury (Feng et al, 2017;Wu and Lipinski, 2019). Autophagy has a double regulating effect in the pathological process in TBI.…”
Section: Traumatic Brain Injury (Tbi)mentioning
confidence: 99%
“…Autophagy is a conserved self-degrading process that regulates the balance between the assembly of cellular components and the degradation of damaged cellular constituents (Wu and Lipinski, 2019). Lysosomal enzymes are involved in autophagic degradation and PPT1 depalmitoylates, the palmitoylated protein in lysosome, prior to their degradation (Koster and Yoshii, 2019).…”
Section: Introductionmentioning
confidence: 99%