ArticleInternational journal of nanomedicine2017
Autophagic flux induced by graphene oxide has a neuroprotective effect against human prion protein fragments.
Article in International journal of nanomedicine, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
10 citing papers in PubMed, 18 citations in OpenAlex.
- FIS1 dependent peripheral fission exacerbates mitochondrial fragmentation and dysfunction in prion diseases.Frontiers in neuroscience · 2026Article
- Rescuing lysosomal/autophagic defects via nanoapproach: implications for lysosomal/autophagic defect-related diseases.Journal of Zhejiang University. Science. B · 2025Review
- Application of Nanomaterials and Related Drug Delivery Systems in Autophagy.Molecules (Basel, Switzerland) · 2024Review
- Preventive effects of nano-graphene oxide against Parkinson's disease via reactive oxygen species scavenging and anti-inflammation.BMB reports · 2023Article
- Review
- Graphene Oxide Ameliorates the Cognitive Impairment Through Inhibiting PI3K/Akt/mTOR Pathway to Induce Autophagy in AD Mouse Model.Neurochemical research · 2021Article
- Calcineurin Activation by Prion Protein Induces Neurotoxicity via Mitochondrial Reactive Oxygen Species.Oxidative medicine and cellular longevity · 2021Article
- The interrupted effect of autophagic flux and lysosomal function induced by graphene oxide in p62-dependent apoptosis of F98 cells.Journal of nanobiotechnology · 2020Article
- Autophagy Modulated by Inorganic Nanomaterials.Theranostics · 2020Review
- Dysregulation of autophagy in the central nervous system of sheep naturally infected with classical scrapie.Scientific reports · 2019Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Graphene oxide (GO) is a nanomaterial with newly developing biological applications. Autophagy is an intracellular degradation system that has been associated with the progression of neurodegenerative disorders. Although induction of autophagic flux by GO has been reported, the underlying signaling pathway in neurodegenerative disorders and how this is involved in neuroprotection remain obscure. We show that GO itself activates autophagic flux in neuronal cells and confers a neuroprotective effect against prion protein (PrP) (106-126)-mediated neurotoxicity. GO can be detected in SK-N-SH neuronal cells, where it triggers autophagic flux signaling. GO-induced autophagic flux prevented PrP (106-126)-induced neurotoxicity in SK-N-SH cells. Moreover, inactivation of autophagic flux blocked GO-induced neuroprotection against prion-mediated mitochondrial neurotoxicity. This is the first study to demonstrate that GO regulates autophagic flux in neuronal cells, and that activation of autophagic flux signals, induced by GO, plays a neuroprotective role against prion-mediated mitochondrial neurotoxicity. These results suggest that the nanomaterial GO may be used to activate autophagic flux and could be used in neuroprotective strategies for treatment of neurodegenerative disorders, including prion diseases.
Indexed as
Identifiers
What OpenQuestion holds
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.