Evidence map›Paper›PMID 30317421›Full record

ArticleNeurochemical research2018

Diallyl Trisulfide Protects Motor Neurons from the Neurotoxic Protein TDP-43 via Activating Lysosomal Degradation and the Antioxidant Response.

Chang Liu, Bingquan Leng, Yi Li, Hong Jiang, Weisong Duan, Yansu Guo, Chunyan Li, Kun Hong

Abstract read
PubMed Publisher
In one paragraph

Article in Neurochemical research, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.4field-weighted citation impact, top 19% of its field
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

14 citing papers in PubMed, 21 citations in OpenAlex.

  1. Review
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  3. Impact of NQO1 dysregulation in CNS disorders.Journal of translational medicine · 2024
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

8 authors at 2 institutions in 1 country.

Chang LiuDepartment of Neurology, Second Hospital of Hebei Medical University, 215 Heping West Road, Shijiazhuang, 050000, Hebei, China.
Bingquan LengDepartment of Neurology, Rizhao Central Hospital, Rizhao, 276800, Shandong, China.
Yi LiDepartment of Neurology, Second Hospital of Hebei Medical University, 215 Heping West Road, Shijiazhuang, 050000, Hebei, China.
Hong JiangDepartment of Neurology, Second Hospital of Hebei Medical University, 215 Heping West Road, Shijiazhuang, 050000, Hebei, China.
Weisong DuanDepartment of Neurology, Second Hospital of Hebei Medical University, 215 Heping West Road, Shijiazhuang, 050000, Hebei, China.
Yansu GuoDepartment of Neurology, Second Hospital of Hebei Medical University, 215 Heping West Road, Shijiazhuang, 050000, Hebei, China.
Chunyan LiDepartment of Neurology, Second Hospital of Hebei Medical University, 215 Heping West Road, Shijiazhuang, 050000, Hebei, China.
Kun HongDepartment of Neurology, Second Hospital of Hebei Medical University, 215 Heping West Road, Shijiazhuang, 050000, Hebei, China. hongkun999@163.com.ORCID http://orcid.org/0000-0001-5264-8034
Hebei Medical University · CNPeople’s Hospital of Rizhao · CN

Funding

Hebei Science and Technology Department 11966122DNational Natural Science Foundation of China 30900460National Natural Science Foundation of China 81171210
6 · The paper itself

Abstract

Amyotrophic lateral sclerosis (ALS) is a rapidly progressive motor neuron disease for which only limited effective therapeutics are available. Currently, TAR DNA-binding protein 43 (TDP-43) is recognized as a pathological and biochemical marker for ALS. Increases in the levels of aggregated or mislocalized forms of TDP-43 might result in ALS pathology. Therefore, clearance pathways for intracellular protein aggregates have been suggested as potential therapeutic targets for the treatment of ALS. Here we report that treatment of motor neuron-like NSC34 cells overexpressing TDP-43 with diallyl trisulfide (DATS) induced neuronal autophagy and lysosomal clearance of TDP-43 and C-terminal TDP-43 fragments. We also observed that the antioxidant transcription factor NF-E2-related factor 2 (Nrf2) was accumulated in the nucleus and the expression of the antioxidant enzymes heme oxygenase1 (HO-1) and NAD(P)H:quinone oxidoreductase (NQO1) was increased. Consequently, DATS suppressed the increase in the levels of reactive oxygen species induced by TDP-43 expression. This study extends the findings of prior reports indicating that lower doses of DATS mediate cell survival in part by inducing autophagy and activating the Nrf2/antioxidant response element pathway.

Indexed as

Allyl CompoundsAntioxidant Response ElementsAntioxidantsCell LineCell SurvivalDNA-Binding ProteinsDose-Response Relationship, DrugHumansLysosomesMotor NeuronsNeuroprotective AgentsReactive Oxygen SpeciesSulfidesAllyl CompoundsAntioxidantsdiallyl trisulfideDNA-Binding ProteinsNeuroprotective AgentsReactive Oxygen SpeciesSulfidesTARDBP protein, humanAmyotrophic lateral sclerosisAutophagyProtein aggregationReactive oxygen speciesTDP-43

Identifiers

PMID30317421
OpenAlexW2896183531

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.