Evidence map›Paper›PMID 40121210›Full record

ArticleNature communications2025

Mitochondria transplantation transiently rescues cerebellar neurodegeneration improving mitochondrial function and reducing mitophagy in mice.

Shu-Jiao Li, Qian-Wen Zheng, Jie Zheng, Jin-Bao Zhang, Hui Liu, Jing-Jing Tie, Kun-Long Zhang, Fei-Fei Wu, Xiao-Dong Li, Shuai Zhang and 3 more

Abstract read
In one paragraph

Article in Nature communications, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed, 1 pooled it
–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

34 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
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  18. Therapeutic Potential of Mitochondrial Transplantation with Focus on DBD.International journal of molecular sciences · 2026
    Review
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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

13 authors.

Shu-Jiao Li *Specific Lab for Mitochondrial Plasticity Underlying Nervous System Diseases, National Teaching Demonstration Center, School of Basic Medicine, Air Force Medical University (Fourth Military Medical University), Xi'an, China.
Qian-Wen Zheng *Department of Hepatobiliary Surgery, Xi-Jing Hospital, Air Force Medical University (Fourth Military Medical University), Xi'an, China.
Jie Zheng *Specific Lab for Mitochondrial Plasticity Underlying Nervous System Diseases, National Teaching Demonstration Center, School of Basic Medicine, Air Force Medical University (Fourth Military Medical University), Xi'an, China.
Jin-Bao Zhang *Department of pediatrics, Xi-Jing Hospital, Air Force Medical University (Fourth Military Medical University), Xi'an, China.
Hui LiuSpecific Lab for Mitochondrial Plasticity Underlying Nervous System Diseases, National Teaching Demonstration Center, School of Basic Medicine, Air Force Medical University (Fourth Military Medical University), Xi'an, China.
Jing-Jing TieSpecific Lab for Mitochondrial Plasticity Underlying Nervous System Diseases, National Teaching Demonstration Center, School of Basic Medicine, Air Force Medical University (Fourth Military Medical University), Xi'an, China.
Kun-Long ZhangSpecific Lab for Mitochondrial Plasticity Underlying Nervous System Diseases, National Teaching Demonstration Center, School of Basic Medicine, Air Force Medical University (Fourth Military Medical University), Xi'an, China.
Fei-Fei WuSpecific Lab for Mitochondrial Plasticity Underlying Nervous System Diseases, National Teaching Demonstration Center, School of Basic Medicine, Air Force Medical University (Fourth Military Medical University), Xi'an, China.
Xiao-Dong LiDepartment of Hepatobiliary Surgery, Xi-Jing Hospital, Air Force Medical University (Fourth Military Medical University), Xi'an, China.
Shuai ZhangSpecific Lab for Mitochondrial Plasticity Underlying Nervous System Diseases, National Teaching Demonstration Center, School of Basic Medicine, Air Force Medical University (Fourth Military Medical University), Xi'an, China.
Xin SunDepartment of pediatrics, Xi-Jing Hospital, Air Force Medical University (Fourth Military Medical University), Xi'an, China. sunxin6@fmmu.edu.cn.ORCID http://orcid.org/0000-0002-5573-551X
Yan-Ling YangDepartment of Hepatobiliary Surgery, Xi-Jing Hospital, Air Force Medical University (Fourth Military Medical University), Xi'an, China. yangyanl@fmmu.edu.cn.ORCID http://orcid.org/0000-0001-8246-1756
Ya-Yun WangSpecific Lab for Mitochondrial Plasticity Underlying Nervous System Diseases, National Teaching Demonstration Center, School of Basic Medicine, Air Force Medical University (Fourth Military Medical University), Xi'an, China. wangyy@fmmu.edu.cn.ORCID http://orcid.org/0000-0002-0397-0390

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cerebellar ataxia is the primary manifestation of cerebellar degenerative diseases, and mitochondrial dysfunction in Purkinje cells (PCs) plays a critical role in disease progression. In this study, we investigated the feasibility of mitochondria transplantation as a potential therapeutic approach to rescue cerebellar neurodegeneration and elucidate the associated mechanisms. We constructed a conditional Drp1 knockout model in PCs (PCKO mice), characterized by progressive ataxia. Drp1 knockout resulted in pervasive and progressive apoptosis of PCs and significant activation of surrounding glial cells. Mitochondrial dysfunction, which triggers mitophagy, is a key pathogenic factor contributing to morphological and functional damage in PCs. Transplanting liver-derived mitochondria into the cerebellum of 1-month-old PCKO mice improved mitochondrial function, reduced mitophagy, delayed apoptosis of PCs, and alleviated cerebellar ataxia for up to 3 weeks. These findings demonstrate that mitochondria transplantation holds promise as a therapeutic approach for cerebellar degenerative diseases.

Indexed as

Cerebellar AtaxiaCerebellumMitochondriaMitophagyAnimalsApoptosisDisease Models, AnimalDynaminsMaleMiceMice, Inbred C57BLMice, KnockoutPurkinje CellsDnm1l protein, mouseDynamins

Identifiers

PMID40121210
PMCPMC11929859

What Socratic holds

Textmetadata
LicenceCC BY-NC-ND
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 Socratic graph.