Evidence map›Paper›PMID 41844629›Full record

ArticleNPJ Parkinson's disease2026

Loss of METTL14 in dopaminergic neurons disrupts ER homeostasis via m6A-dependent regulation of Atp2a3 mRNA: Implications for Parkinson's Disease.

Yan Teng, Zhihao Liu, Fan Wei, Qin Tang, Manjun Li, Xingmin Chen, Jin Yi, Shu He, Jianli Xu, Yuqing Hang and 5 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in NPJ Parkinson's disease, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
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

1 citing paper in PubMed.

  1. 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

15 authors.

Yan Teng *Department of Neurology & Institute of Neurology, Sichuan Provincial People's Hospital, University of Electronic Science and Technology of China, Chengdu, Sichuan, 610054, China.
Zhihao Liu *School of Medicine, University of Electronic Science and Technology of China, Chengdu, Sichuan, 610054, China.
Fan Wei *School of Medicine, University of Electronic Science and Technology of China, Chengdu, Sichuan, 610054, China.
Qin Tang *School of Medicine, University of Electronic Science and Technology of China, Chengdu, Sichuan, 610054, China.
Manjun LiSchool of Medicine, University of Electronic Science and Technology of China, Chengdu, Sichuan, 610054, China.
Xingmin ChenSchool of Medicine, University of Electronic Science and Technology of China, Chengdu, Sichuan, 610054, China.
Jin YiDepartment of Neurology & Institute of Neurology, Sichuan Provincial People's Hospital, University of Electronic Science and Technology of China, Chengdu, Sichuan, 610054, China.
Shu HeDepartment of Neurology & Institute of Neurology, Sichuan Provincial People's Hospital, University of Electronic Science and Technology of China, Chengdu, Sichuan, 610054, China.
Jianli XuDepartment of Neurology & Institute of Neurology, Sichuan Provincial People's Hospital, University of Electronic Science and Technology of China, Chengdu, Sichuan, 610054, China.
Yuqing HangSchool of Medicine, University of Electronic Science and Technology of China, Chengdu, Sichuan, 610054, China.
Kaifang WangSchool of Medicine, University of Electronic Science and Technology of China, Chengdu, Sichuan, 610054, China.
Yanzhuo LiuSchool of Medicine, University of Electronic Science and Technology of China, Chengdu, Sichuan, 610054, China.
Haisong JiangDepartment of Neurology & Institute of Neurology, Sichuan Provincial People's Hospital, University of Electronic Science and Technology of China, Chengdu, Sichuan, 610054, China. jhsarchangle@hotmail.com.
Weidong LeDepartment of Neurology & Institute of Neurology, Sichuan Provincial People's Hospital, University of Electronic Science and Technology of China, Chengdu, Sichuan, 610054, China. wdle@sibs.ac.cn.
Lu YangDepartment of Neurology & Institute of Neurology, Sichuan Provincial People's Hospital, University of Electronic Science and Technology of China, Chengdu, Sichuan, 610054, China. lyang@uestc.edu.cn.

Funding

Clinical Medicine Discipline Development Fund,School of medicine,UESTC YXYLCJJ202402015National Natural Science Foundation of China 32220103006National Natural Science Foundation of China 81601125the Department of Science and Technology of Sichuan Province 2022YFS0597the Department of Science and Technology of Sichuan Province 2025ZNSFSC1743
6 · The paper itself

Abstract

Dopaminergic (DA) neurons are highly susceptible to endoplasmic reticulum (ER) burden and redox imbalance, which drive their degeneration and contribute to Parkinson's disease (PD) pathogenesis. Previous work established METTL14-mediated N6-methyladenosine (m6A) modification as critical for dopaminergic (DA) neuron survival. Here, we delineate the underlying mechanism by which m6A dysregulation triggers neurodegeneration through the post-transcriptional modulation of key target genes. Using Mettl14 conditional knockout mice, we identified the ER calcium channel ATP2A3-a key calcium homeostasis regulator and known PD biomarker-as a major target of METTL14. METTL14 deficiency significantly reduced ATP2A3 expression, thereby exacerbating ER homeostasis and oxidative stress, ultimately leading to DA neuronal death. Restoring METTL14 in vivo alleviates motor deficits and neurodegeneration. Our findings reveal that m6A-mediated regulation of ATP2A3 bridges RNA epigenetic dysregulation to PD pathogenesis, highlighting this axis as a potential therapeutic target in this disease.

Identifiers

PMID41844629
PMCPMC13144520

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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.