Evidence map›Paper›PMID 34026326›Full record

ArticleMolecular therapy. Nucleic acids2021

miR-204 silencing reduces mitochondrial autophagy and ROS production in a murine AD model via the TRPML1-activated STAT3 pathway.

Lu Zhang, Yu Fang, Xinyu Zhao, Yake Zheng, Yunqing Ma, Shuang Li, Zhi Huang, Lihao Li

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 41 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
41citing papers in PubMed, 2 pooled it
9.1field-weighted citation impact, top 1% 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

41 citing papers in PubMed, 2 syntheses or guidelines pooled it, 70 citations in OpenAlex.

  1. Pooled it
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  11. Inter-Organellar CaCells · 2025
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  13. Autophagy: a double-edged sword in ischemia-reperfusion injury.Cellular & molecular biology letters · 2025
    Review
  14. Mitochondrial dysfunction in Alzheimer's disease: Guiding the path to targeted therapies.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2025
    Review
  15. Article
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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 1 institution in 1 country.

Lu ZhangDepartment of Neurology, the First Affiliated Hospital of Zhengzhou University, Zhengzhou 450052, P.R. China.
Yu FangICU, The First Affiliated Hospital of Zhengzhou University, Zhengzhou 450052, P.R. China.
Xinyu ZhaoDepartment of Neurology, the First Affiliated Hospital of Zhengzhou University, Zhengzhou 450052, P.R. China.
Yake ZhengDepartment of Neurology, the First Affiliated Hospital of Zhengzhou University, Zhengzhou 450052, P.R. China.
Yunqing MaDepartment of Neurology, the First Affiliated Hospital of Zhengzhou University, Zhengzhou 450052, P.R. China.
Shuang LiDepartment of Neurology, the First Affiliated Hospital of Zhengzhou University, Zhengzhou 450052, P.R. China.
Zhi HuangDepartment of Neurology, the First Affiliated Hospital of Zhengzhou University, Zhengzhou 450052, P.R. China.
Lihao LiDepartment of Neurology, the First Affiliated Hospital of Zhengzhou University, Zhengzhou 450052, P.R. China.
First Affiliated Hospital of Zhengzhou University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Mitochondrial dysfunction is an early feature of Alzheimer's disease (AD), whereby accumulation of damaged mitochondria in conjunction with impaired mitophagy contributes to neurodegeneration. Various non-transcribed microRNAs (miRNAs) are involved in this process. In the present study, we aimed to decipher the participation of miR-204 in a murine AD model. Primary hippocampal neurons were isolated from mice and treated with β-amyloid 1-42 (Aβ1-42) to establish a cell model of AD. Dichloro-dihydro-fluorescein diacetate and dihydrorhodamine 123 staining assays were performed to measure total reactive oxygen species (ROS) and mitochondrial ROS production in neurons, and MitoSOX staining was done to analyze mitochondrial ROS production in hippocampus. Furthermore, mitochondrial autophagy was observed in hippocampus from amyloid precursor protein/pesenilin-1 AD modeled mice, and their cognitive function was assessed by Morris water maze. Mitochondrial damage, ROS production, and mitochondrial autophagy were observed in AD cell model induced by Aβ1-42. In AD, signal transducer and activator of transcription 3 (STAT3) and transient receptor potential mucolipin-1 (TRPML1) expression was downregulated, although miR-204 expression was upregulated. TRPML1 overexpression, downregulation of miR-204, or STAT3 pathway activation reduced the Aβ1-42-induced mitochondrial damage, along with ROS production and mitochondrial autophagy

Indexed as

Alzheimer’s diseaseAβ1-42hippocampal neuronsmicroRNA-204mitochondrial autophagyreactive oxygen speciessignal transducer and activator of transcription 3transient receptor potential mucolipin-1

Identifiers

PMID34026326
PMCPMC8121631
OpenAlexW3130534574

What OpenQuestion holds

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Registered trials

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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.