Evidence map›Paper›PMID 39764629›Full record

ArticleCNS neuroscience & therapeutics2025

Impact of LITAF on Mitophagy and Neuronal Damage in Epilepsy via MCL-1 Ubiquitination.

Fuli Min, Zhaofei Dong, Shuisheng Zhong, Ze Li, Hong Wu, Sai Zhang, Linming Zhang, Tao Zeng

Abstract read
In one paragraph

Article in CNS neuroscience & therapeutics, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

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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

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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

2 citing papers in PubMed.

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4 · The record

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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.

Fuli MinDepartment of Neurology, School of Medicine, Guangzhou First People's Hospital, South China University of Technology, Guangzhou, China.
Zhaofei DongDepartment of Neurology, the Eighth Affiliated Hospital, Sun Yat-Sen University, Shenzhen, China.
Shuisheng ZhongDepartment of Neurology, Guangdong Sanjiu Brain Hospital, Guangzhou, China.
Ze LiDepartment of Neurology, School of Medicine, Guangzhou First People's Hospital, South China University of Technology, Guangzhou, China.
Hong WuDepartment of Neurology, School of Medicine, Guangzhou First People's Hospital, South China University of Technology, Guangzhou, China.
Sai ZhangDepartment of Neurology, School of Medicine, Guangzhou First People's Hospital, South China University of Technology, Guangzhou, China.
Linming ZhangDepartment of Neurology, The First Affliated Hospital of Kunming Medical University, Kunming, China.
Tao ZengDepartment of Neurology, School of Medicine, Guangzhou First People's Hospital, South China University of Technology, Guangzhou, China.

Funding

Futian Healthcare Research Project FTWS2023083National Natural Science Foundation of China 82001370National Natural Science Foundation of China 82060252Natural Science Foundation of Guangdong Province 2021A1515220116Science and Technology Program of Guangzhou 202201010071Science and Technology Program of Guangzhou 2023A03J0960The Major Science and Technology Special Project of Yunnan Province 202102AA100061
6 · The paper itself

Abstract

objectiveThis study aims to investigate how the E3 ubiquitin ligase LITAF influences mitochondrial autophagy by modulating MCL-1 ubiquitination, and its role in the development of epilepsy.

methodsEmploying single-cell RNA sequencing (scRNA-seq) to analyze brain tissue from epilepsy patients, along with high-throughput transcriptomics, we identified changes in gene expression. This was complemented by in vivo and in vitro experiments, including protein-protein interaction (PPI) network analysis, western blotting, and behavioral assessments in mouse models.

resultsNeuronal cells in epilepsy patients exhibited significant gene expression alterations, with increased activity in apoptosis-related pathways and decreased activity in neurotransmitter-related pathways. LITAF was identified as a key upregulated factor, inhibiting mitochondrial autophagy by promoting MCL-1 ubiquitination, leading to increased neuronal damage. Knockdown experiments in mouse models further confirmed that LITAF facilitates MCL-1 ubiquitination, aggravating neuronal injury.

conclusionOur findings demonstrate that LITAF regulates MCL-1 ubiquitination, significantly impacting mitochondrial autophagy and contributing to neuronal damage in epilepsy. Targeting LITAF and its downstream mechanisms may offer a promising therapeutic strategy for managing epilepsy.

Indexed as

EpilepsyMitophagyMyeloid Cell Leukemia Sequence 1 ProteinNeuronsTranscription FactorsUbiquitinationAnimalsFemaleHumansMaleMiceMice, Inbred C57BLNuclear ProteinsUbiquitin-Protein LigasesMCL1 protein, humanMyeloid Cell Leukemia Sequence 1 ProteinNuclear ProteinsTranscription FactorsUbiquitin-Protein LigasesepilepsyLPS‐induced TNF‐alpha factorMCL1mitochondrial autophagyneuroprotectionubiquitination regulation

Identifiers

PMID39764629
PMCPMC11705406

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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.