Evidence map›Paper›PMID 33575111›Full record

ArticleMolecular therapy. Nucleic acids2021

miR-351-5p/Miro2 axis contributes to hippocampal neural progenitor cell death via unbalanced mitochondrial fission.

Ha-Na Woo, Sujeong Park, Hae Lin Kim, Min-Kyo Jung, Chan-Gi Pack, Jinsu Park, Yoonsuk Cho, Dong-Gyu Jo, Dong Kyu Kim, Inhee Mook-Jung and 2 more

Open access · goldAbstract read
In one paragraph

Article in Molecular therapy. Nucleic acids, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed, 2 pooled it
1.1field-weighted citation impact, top 24% 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

21 citing papers in PubMed, 2 syntheses or guidelines pooled it, 24 citations in OpenAlex.

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  18. The Potential Role of miRNA-Regulated Autophagy in Alzheimer's Disease.International journal of molecular sciences · 2022
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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

12 authors at 6 institutions in 1 country.

Ha-Na WooDepartment of Microbiology, University of Ulsan College of Medicine, Seoul 05505, Korea.
Sujeong ParkDepartment of Microbiology, University of Ulsan College of Medicine, Seoul 05505, Korea.
Hae Lin KimDepartment of Microbiology, University of Ulsan College of Medicine, Seoul 05505, Korea.
Min-Kyo JungNeural Circuits Group, Korea Brain Research Institute, Daegu, Korea.
Chan-Gi PackAsan Institute for Life Sciences, Asan Medical Center, University of Ulsan College of Medicine, Seoul, Korea.
Jinsu ParkSchool of Pharmacy, Sungkyunkwan University, Suwon, Korea.
Yoonsuk ChoSchool of Pharmacy, Sungkyunkwan University, Suwon, Korea.
Dong-Gyu JoSchool of Pharmacy, Sungkyunkwan University, Suwon, Korea.
Dong Kyu KimDepartment of Biomedical Sciences, College of Medicine, Seoul National University, Seoul, Korea.
Inhee Mook-JungDepartment of Biomedical Sciences, College of Medicine, Seoul National University, Seoul, Korea.
Seong Who KimBio-Medical Institute of Technology, Asan Medical Center, Seoul 05505, Korea.
Heuiran LeeDepartment of Microbiology, University of Ulsan College of Medicine, Seoul 05505, Korea.
University of Ulsan · KRSungkyunkwan University · KRSeoul National University · KRAsan Medical Center · KRKorea Brain Research Institute · KRUlsan College · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Adult hippocampal neurogenesis supports the structural and functional plasticity of the brain, while its decline is associated with neurodegeneration common in Alzheimer's disease (AD). Although the dysregulation of certain microRNAs (miRNAs) in AD have been observed, the effects of miRNAs on hippocampal neurogenesis are largely unknown. In this study, we demonstrated miR-351-5p as a causative factor in hippocampal neural progenitor cell death through modulation of the mitochondrial guanosine triphosphatase (GTPase), Miro2. Downregulation of Miro2 by siMiro2 induced cell death, similar to miR-351-5p, whereas ectopic Miro2 expression using an adenovirus abolished these effects. Excessively fragmented mitochondria and dysfunctional mitochondria were indexed by decreased mitochondrial potential, and increased reactive oxygen species were identified in miR-351-5p-induced cell death. Moreover, subsequent induction of mitophagy via Pink1 and Parkin was observed in the presence of miR-351-5p and siMiro2. The suppression of mitochondrial fission by Mdivi-1 completely inhibited cell death by miR-351-5p. miR-351-5p expression increased whereas the level of Miro2 decreased in the hippocampus of AD model mice, emulating expression in AD patients. Collectively, the data indicate the mitochondrial fission and accompanying mitophagy by miR-351-5p/Miro2 axis as critical in hippocampal neural progenitor cell death, and a potential therapeutic target in AD.

Indexed as

Alzheimer’s diseaseautophagycell deathhippocampal neural progenitor cellsmiRNA-351-5pMiro GTPasemitophagy

Identifiers

PMID33575111
PMCPMC7848773
OpenAlexW3116953426

What OpenQuestion holds

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LicenceCC BY-NC-ND
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.