ArticleFrontiers in neuroscience2017
Sequestosome 1 Deficiency Delays, but Does Not Prevent Brain Damage Formation Following Acute Brain Injury in Adult Mice.
Article in Frontiers in neuroscience, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers, 2 of them syntheses that pooled it.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
7 citing papers in PubMed, 2 syntheses or guidelines pooled it, 10 citations in OpenAlex.
- Traumatic MicroRNAs: Deconvolving the Signal After Severe Traumatic Brain Injury.Cellular and molecular neurobiology · 2023Pooled it
- Old and Promising Markers Related to Autophagy in Traumatic Brain Injury.International journal of molecular sciences · 2022Pooled it
- Traumatic brain injury and autophagy: a pilot study about the immunohistochemical expression of LC3B, Beclin 1, p62, and LAMP2A in human autoptic samples.Frontiers in molecular neuroscience · 2025Article
- Autophagy machinery plays an essential role in traumatic brain injury-induced apoptosis and its related behavioral abnormalities in mice: focus onFrontiers in physiology · 2023Article
- Posttraumatic midazolam administration does not influence brain damage after experimental traumatic brain injury.BMC anesthesiology · 2022Article
- Royal Jelly as an Intelligent Anti-Aging Agent-A Focus on Cognitive Aging and Alzheimer's Disease: A Review.Antioxidants (Basel, Switzerland) · 2020Review
- Mitochondrial Degeneration and Autophagy Associated With Delayed Effects of Radiation in the Mouse Brain.Frontiers in aging neuroscience · 2019Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Neuronal degeneration following traumatic brain injury (TBI) leads to intracellular accumulation of dysfunctional proteins and organelles. Autophagy may serve to facilitate degradation to overcome protein debris load and therefore be an important pro-survival factor. On the contrary, clearing may serve as pro-death factor by removal of essential or required proteins involved in pro-survival cascades. Sequestosome 1 (SQSTM1/p62) is a main regulator of the autophagic pathway that directs ubiquinated cargoes to autophagosomes for degradation. We show that SQSTM1 protein levels are suppressed 24 h and by trend 5 days after trauma. In line with these data the expression of
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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.