ArticleCell death & disease2018
Impaired autophagic flux is associated with the severity of trauma and the role of A
Article in Cell death & disease, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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Who cites it
30 citing papers in PubMed, 57 citations in OpenAlex.
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- RACK1 promotes autophagy via the PERK signaling pathway to protect against traumatic brain injury in rats.CNS neuroscience & therapeutics · 2024Article
- Inhibition of the interaction between microglial adenosine 2A receptor and NLRP3 inflammasome attenuates neuroinflammation posttraumatic brain injury.CNS neuroscience & therapeutics · 2024Article
- HSPB2 facilitates neural regeneration through autophagy for sensorimotor recovery after traumatic brain injury.JCI insight · 2023Article
- Overexpressed ski efficiently promotes neurorestoration, increases neuronal regeneration, and reduces astrogliosis after traumatic brain injury.Gene therapy · 2023Article
- Involvement of Autophagy in the Protective Effects of Ginsenoside Rb1 in a Rat Model of Traumatic Brain Injury.European journal of drug metabolism and pharmacokinetics · 2022Article
- Urolithin A alleviates blood-brain barrier disruption and attenuates neuronal apoptosis following traumatic brain injury in mice.Neural regeneration research · 2022Article
- Cerebrospinal fluid purinomics as a biomarker approach to predict outcome after severe traumatic brain injury.Journal of neurochemistry · 2022Article
- Ablation of GSDMD Attenuates Neurological Deficits and Neuropathological Alterations After Traumatic Brain Injury.Frontiers in cellular neuroscience · 2022Article
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- Nanomaterial-mediated autophagy: coexisting hazard and health benefits in biomedicine.Particle and fibre toxicology · 2020Review
- Therapeutic effects of rapamycin and surgical decompression in a rabbit spinal cord injury model.Cell death & disease · 2020Article
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Corrections and comments
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Authors and funding
9 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Recent studies have shown that after traumatic brain injury (TBI), the number of autophagosomes is markedly increased in brain cells surrounding the wound; however, whether autophagy is enhanced or suppressed by TBI remains controversial. In our study, we used a controlled cortical impact system to establish models of mild, moderate and severe TBI. In the mild TBI model, the levels of autophagy-related protein 6 (Beclin1) and autophagy-related protein 12 (ATG12)-autophagy-related protein 5 (ATG5) conjugates were increased, indicating the enhanced initiation of autophagy. Furthermore, the level of the autophagic substrate sequestosome 1 (SQSTM1) was decreased in the ipsilateral cortex. This result, together with the results observed in tandem mRFP-GFP-LC3 adeno-associated virus (AAV)-infected mice, indicates that autophagosome clearance was also increased after mild TBI. Conversely, following moderate and severe TBI, there was no change in the initiation of autophagy, and autophagosome accumulation was observed. Next, we used chloroquine (CQ) to artificially impair autophagic flux in the injured cortex of the mild TBI model and found that the severity of trauma was obviously exacerbated. In addition, autophagic flux and trauma severity were significantly improved in adenosine A
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.