Evidence map›Paper›PMID 31440210›Full record

ArticleFrontiers in endocrinology2019

Reduction of Mitophagy-Related Oxidative Stress and Preservation of Mitochondria Function Using Melatonin Therapy in an HT22 Hippocampal Neuronal Cell Model of Glutamate-Induced Excitotoxicity.

Dan-Dan Wang, Mei-Fang Jin, Dong-Jing Zhao, Hong Ni

Open access · goldAbstract read
In one paragraph

Article in Frontiers in endocrinology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
1.6field-weighted citation impact, top 17% 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

24 citing papers in PubMed, 38 citations in OpenAlex.

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  10. Investigation into Antioxidant Mechanism ofFoods (Basel, Switzerland) · 2024
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  17. International journal of molecular sciences · 2022
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  20. Antioxidants (Basel, Switzerland) · 2021
    Article
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

4 authors at 1 institution in 1 country.

Dan-Dan WangDivision of Brain Science, Institute of Pediatric Research, Children's Hospital of Soochow University, Suzhou, China.
Mei-Fang JinDivision of Brain Science, Institute of Pediatric Research, Children's Hospital of Soochow University, Suzhou, China.
Dong-Jing ZhaoDivision of Brain Science, Institute of Pediatric Research, Children's Hospital of Soochow University, Suzhou, China.
Hong NiDivision of Brain Science, Institute of Pediatric Research, Children's Hospital of Soochow University, Suzhou, China.
Soochow University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Recent evidence indicates that autophagy-mediated mitochondrial homeostasis is crucial for oxidative stress-related brain damage and repair. The highest concentration of melatonin is in the mitochondria of cells, and melatonin exhibits well-known antioxidant properties. We investigated the impact and mechanism involved in mitochondrial function and the mitochondrial oxidative stress/autophagy regulator parameters of glutamate cytotoxicity in mouse HT22 hippocampal neurons. We tested the hypothesis that melatonin confers neuroprotective effects via protecting against mitochondrial impairment and mitophagy. Cells were divided into four groups: the control group, melatonin alone group, glutamate injury group, and melatonin pretreatment group. We found that glutamate induced significant changes in mitochondrial function/oxidative stress-related parameters. Leptin administration preserved mitochondrial function, and this effect was associated with increased superoxide dismutase, glutathione (GSH), and mitochondrial membrane potential and decreased GSSG (oxidized glutathione) and mitochondrial reactive oxygen species. Melatonin significantly reduced the fluorescence intensity of mitophagy via the Beclin-1/Bcl-2 pathway, which involves Beclin-1 and Bcl-2 proteins. The mitophagy inhibitor CsA corrected these glutamate-induce changes, as measured by the fluorescence intensity of Mitophagy-Tracker Red CMXROS, mitochondrial ROS, and mitochondrial membrane potential changes. These findings indicate that melatonin exerts neuroprotective effects against glutamate-induced excitotoxicity by reducing mitophagy-related oxidative stress and maintaining mitochondrial function.

Indexed as

glutamateHT22melatoninmitochondriamitophagy

Identifiers

PMID31440210
PMCPMC6694460
OpenAlexW2963534313

What OpenQuestion holds

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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.