Evidence map›Paper›PMID 40624018›Full record

ArticleCell death & disease2025

Homocysteine interferes with Ndufa1 leading to mitochondrial dysfunction through repression of the NAD

Gaoshang Chai, Yuming Mao, Juan Gong, Shuguang Bi, Yuqi Zhang, Jiajun Wu, Liu Yang, Tianlong Gao, Haitian Fu, Chunjing Yu and 8 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cell death & disease, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing 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

4 citing papers in PubMed.

  1. Review
  2. Article
  3. 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

18 authors.

Gaoshang Chai *Department of Fundamental Medicine, Wuxi School of Medicine, Jiangnan University, Wuxi, Jiangsu, China. chaigaoshang@jiangnan.edu.cn.ORCID http://orcid.org/0000-0002-1943-3717
Yuming Mao *Department of Fundamental Medicine, Wuxi School of Medicine, Jiangnan University, Wuxi, Jiangsu, China.
Juan GongDepartment of Fundamental Medicine, Wuxi School of Medicine, Jiangnan University, Wuxi, Jiangsu, China.
Shuguang BiDepartment of Fundamental Medicine, Wuxi School of Medicine, Jiangnan University, Wuxi, Jiangsu, China.
Yuqi ZhangDepartment of Fundamental Medicine, Wuxi School of Medicine, Jiangnan University, Wuxi, Jiangsu, China.
Jiajun WuDepartment of Electrophysiology, Wuhan Children's Hospital (Wuhan Maternal and Children's Healthcare Center), Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei, China.
Liu YangDepartment of Fundamental Medicine, Wuxi School of Medicine, Jiangnan University, Wuxi, Jiangsu, China.
Tianlong GaoDepartment of Fundamental Medicine, Wuxi School of Medicine, Jiangnan University, Wuxi, Jiangsu, China.
Haitian FuNuclear Medicine Center, Jiangnan University Affiliated Hospital, Wuxi, Jiangsu, China.
Chunjing YuNuclear Medicine Center, Jiangnan University Affiliated Hospital, Wuxi, Jiangsu, China.
Caili RenDepartment of Neurology, The Affiliated Mental Health Center of Jiangnan University, Wuxi, Jiangsu, China.
Guofu ZhangDepartment of Clinical Psychiatry, The Affiliated Mental Health Center of Jiangnan University, Wuxi, Jiangsu, China.ORCID http://orcid.org/0009-0008-5027-556X
Xuming ZhuDepartment of Laboratory Medicine, The Affiliated Wuxi People's Hospital of Nanjing Medical University, Wuxi, Jiangsu, China.
Xin GuanScience Center for Future Foods, Jiangnan University, Wuxi, Jiangsu, China.
Haoting YuDepartment of Fundamental Medicine, Wuxi School of Medicine, Jiangnan University, Wuxi, Jiangsu, China.
Caijing TangDepartment of Fundamental Medicine, Wuxi School of Medicine, Jiangnan University, Wuxi, Jiangsu, China.
Yunjuan NieDepartment of Fundamental Medicine, Wuxi School of Medicine, Jiangnan University, Wuxi, Jiangsu, China.
Haitao YuDepartment of Fundamental Medicine, Wuxi School of Medicine, Jiangnan University, Wuxi, Jiangsu, China. yu_haitao@jiangnan.edu.cn.ORCID http://orcid.org/0000-0002-0302-998X

Funding

National Natural Science Foundation of China (National Science Foundation of China) 81601121National Natural Science Foundation of China (National Science Foundation of China) 82401671
6 · The paper itself

Abstract

Mitochondrial defects are early pathological changes in neurodegenerative disease (ND). Homocysteine (Hcy) is an independent risk factor for ND. However, whether and how Hcy induces mitochondrial defects during the process of neurodegeneration is unclear. Here, we revealed that Hcy interfered with mitochondrial oxidative phosphorylation (OXPHOS) by inhibiting the mitochondrial electron transport chain (ETC) complex I, resulting in increased levels of reactive oxygen species (ROS) in the hippocampus of rats. Specifically, Hcy suppressed Ndufa1 expression, which is essential for complex I assembly and activation, by interfering with its transcription factor Creb1. Moreover, we found that Hcy induced neurodegeneration-like pathological changes in mitochondria in the brain via the inhibition of the NAD

Indexed as

BrainElectron Transport Complex IHomocysteineHyperhomocysteinemiaMitochondriaNADNeurodegenerative DiseasesSirtuin 1AnimalsHippocampusMaleMitophagyOxidative PhosphorylationRatsRats, Sprague-DawleyReactive Oxygen SpeciesElectron Transport Complex IHomocysteineNADReactive Oxygen SpeciesSirt1 protein, ratSirtuin 1

Identifiers

PMID40624018
PMCPMC12234694

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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.