Evidence map›Paper›PMID 37488867›Full record

ArticleNeural regeneration research2024

CHCHD2 Thr61Ile mutation impairs F1F0-ATPase assembly in

Xiang Chen, Yuwan Lin, Zhiling Zhang, Yuting Tang, Panghai Ye, Wei Dai, Wenlong Zhang, Hanqun Liu, Guoyou Peng, Shuxuan Huang and 7 more

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Neural regeneration research, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
0.9field-weighted citation impact, top 25% 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

5 citing papers in PubMed, 6 citations in OpenAlex.

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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

17 authors at 4 institutions in 1 country.

Xiang ChenDepartment of Neurology, The First Affiliated Hospital of Guangzhou Medical University, Guangzhou, Guangdong Province, China.
Yuwan LinDepartment of Neurology, The First Affiliated Hospital of Guangzhou Medical University, Guangzhou, Guangdong Province, China.
Zhiling ZhangDepartment of Neurology, The First Affiliated Hospital of Guangzhou Medical University, Guangzhou, Guangdong Province, China.
Yuting TangDepartment of Neurology, The First Affiliated Hospital of Guangzhou Medical University, Guangzhou, Guangdong Province, China.
Panghai YeDepartment of Neurology, The First Affiliated Hospital of Guangzhou Medical University, Guangzhou, Guangdong Province, China.
Wei DaiDepartment of Neurology, The First Affiliated Hospital of Guangzhou Medical University, Guangzhou, Guangdong Province, China.
Wenlong ZhangDepartment of Neurology, The First Affiliated Hospital of Guangzhou Medical University, Guangzhou, Guangdong Province, China.
Hanqun LiuDepartment of Neurology, The First Affiliated Hospital of Guangzhou Medical University, Guangzhou, Guangdong Province, China.
Guoyou PengDepartment of Neurology, The First Affiliated Hospital of Guangzhou Medical University, Guangzhou, Guangdong Province, China.
Shuxuan HuangDepartment of Neurology, The People's Hospital of Guangxi Zhuang Autonomous Region, Nanning, Guangxi Zhuang Autonomous Region, China.
Jiewen QiuDepartment of Neurology, The First Affiliated Hospital of Guangzhou Medical University, Guangzhou, Guangdong Province, China.
Wenyuan GuoDepartment of Neurology, The First Affiliated Hospital of Guangzhou Medical University, Guangzhou, Guangdong Province, China.
Xiaoqin ZhuSchool of Basic Medical Sciences, Guangzhou Medical University, Guangzhou, Guangdong Province, China.
Zhuohua WuDepartment of Neurology, The First Affiliated Hospital of Guangzhou Medical University, Guangzhou, Guangdong Province, China.
Yaoyun KuangDepartment of Neurology, The First Affiliated Hospital of Guangzhou Medical University, Guangzhou, Guangdong Province, China.
Pingyi XuDepartment of Neurology, The First Affiliated Hospital of Guangzhou Medical University, Guangzhou, Guangdong Province, China.
Miaomiao ZhouDepartment of Neurology, The First Affiliated Hospital of Guangzhou Medical University, Guangzhou, Guangdong Province; Department of Neurology, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Guangzhou Medical University · CNFirst Affiliated Hospital of Guangzhou Medical University · CNShanghai Jiao Tong University · CNThe People's Hospital of Guangxi Zhuang Autonomous Region · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Mitochondrial dysfunction is a significant pathological alteration that occurs in Parkinson's disease (PD), and the Thr61Ile (T61I) mutation in coiled-coil helix coiled-coil helix domain containing 2 (CHCHD2), a crucial mitochondrial protein, has been reported to cause Parkinson's disease. F1F0-ATPase participates in the synthesis of cellular adenosine triphosphate (ATP) and plays a central role in mitochondrial energy metabolism. However, the specific roles of wild-type (WT) CHCHD2 and T61I-mutant CHCHD2 in regulating F1F0-ATPase activity in Parkinson's disease, as well as whether CHCHD2 or CHCHD2 T61I affects mitochondrial function through regulating F1F0-ATPase activity, remain unclear. Therefore, in this study, we expressed WT CHCHD2 and T61I-mutant CHCHD2 in an MPP

Indexed as

ATP synthase (F1F0-ATPase)coiled-coil helix coiled-coil helix domain containing 2dopaminergic neuronmitochondrial dysfunctionneurodegenerationoligomycin sensitivity-conferring proteinParkinson’s diseaseT61I mutationtyrosine hydroxylase

Identifiers

PMID37488867
PMCPMC10479855
OpenAlexW4382139072

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.