Evidence map›Paper›PMID 33644049›Full record

ArticleFrontiers in cell and developmental biology2021

NADPH and Mito-Apocynin Treatment Protects Against KA-Induced Excitotoxic Injury Through Autophagy Pathway.

Na Liu, Miao-Miao Lin, Si-Si Huang, Zi-Qi Liu, Jun-Chao Wu, Zhong-Qin Liang, Zheng-Hong Qin, Yan Wang

Open access · goldAbstract read
In one paragraph

Article in Frontiers in cell and developmental biology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed, 1 pooled it
1.6field-weighted citation impact, top 18% 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

22 citing papers in PubMed, 1 synthesis or guideline pooled it, 31 citations in OpenAlex.

  1. Pooled it
  2. The emerging roles of disulfidptosis in cancer.Apoptosis : an international journal on programmed cell death · 2026
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  15. Disulfidptosis: A new type of cell death.Apoptosis : an international journal on programmed cell death · 2024
    Review
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  19. Review
  20. The role of TIGAR in nervous system diseases.Frontiers in aging neuroscience · 2022
    Review
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 1 institution in 1 country.

Na LiuDepartment of Pharmacology and Laboratory of Aging and Nervous Diseases and Jiangsu Key Laboratory of Neuropsychiatric Diseases, College of Pharmaceutical Sciences, Soochow University, Suzhou, China.
Miao-Miao LinDepartment of Pharmacology and Laboratory of Aging and Nervous Diseases and Jiangsu Key Laboratory of Neuropsychiatric Diseases, College of Pharmaceutical Sciences, Soochow University, Suzhou, China.
Si-Si HuangDepartment of Pharmacology and Laboratory of Aging and Nervous Diseases and Jiangsu Key Laboratory of Neuropsychiatric Diseases, College of Pharmaceutical Sciences, Soochow University, Suzhou, China.
Zi-Qi LiuDepartment of Pharmacology and Laboratory of Aging and Nervous Diseases and Jiangsu Key Laboratory of Neuropsychiatric Diseases, College of Pharmaceutical Sciences, Soochow University, Suzhou, China.
Jun-Chao WuDepartment of Pharmacology and Laboratory of Aging and Nervous Diseases and Jiangsu Key Laboratory of Neuropsychiatric Diseases, College of Pharmaceutical Sciences, Soochow University, Suzhou, China.
Zhong-Qin LiangDepartment of Pharmacology and Laboratory of Aging and Nervous Diseases and Jiangsu Key Laboratory of Neuropsychiatric Diseases, College of Pharmaceutical Sciences, Soochow University, Suzhou, China.
Zheng-Hong QinDepartment of Pharmacology and Laboratory of Aging and Nervous Diseases and Jiangsu Key Laboratory of Neuropsychiatric Diseases, College of Pharmaceutical Sciences, Soochow University, Suzhou, China.
Yan WangDepartment of Pharmacology and Laboratory of Aging and Nervous Diseases and Jiangsu Key Laboratory of Neuropsychiatric Diseases, College of Pharmaceutical Sciences, Soochow University, Suzhou, China.
Soochow University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

aimPrevious research recognizes that NADPH can produce reduced glutathione (GSH) as a coenzyme and produce ROS as a substrate of NADPH oxidase (NOX). Besides, excessive activation of glutamate receptors results in mitochondrial impairment. The study aims at spelling out the effects of NADPH and Mito-apocynin, a NOX inhibitor which specifically targets the mitochondria, on the excitotoxicity induced by Kainic acid (KA) and its mechanism.

methodsThe

resultsIn this study, we have successfully established excitotoxic model by KA

conclusionIn summary, combined administration of NADPH and NOX inhibitors offers better neuroprotection by reducing NADPH as a NOX substrate to generate ROS. The combined use of NADPH and Mito-apocynin can better restore neurons and mitochondrial function through autophagy pathway.

Indexed as

autophagyexcitotoxicityMito-apocyninmitochondriaNADPHNOXROS

Identifiers

PMID33644049
PMCPMC7905037
OpenAlexW3127826314

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.