Evidence map›Paper›PMID 37424172›Full record

ReviewCNS neuroscience & therapeutics2023

Intercellular mitochondrial transfer in the brain, a new perspective for targeted treatment of central nervous system diseases.

Ziang Geng, Shu Guan, Siqi Wang, Zhongxue Yu, Tiancong Liu, Shaonan Du, Chen Zhu

Open access · goldAbstract readReview
In one paragraph

Review in CNS neuroscience & therapeutics, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed, 1 pooled it
6.2field-weighted citation impact, top 3% 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

35 citing papers in PubMed, 1 synthesis or guideline pooled it, 40 citations in OpenAlex.

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  15. Mitochondrial Metabolism in T-Cell Exhaustion.International journal of molecular sciences · 2025
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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

7 authors at 2 institutions in 1 country.

Ziang GengDepartment of Neurosurgery, Shengjing Hospital of China Medical University, Shenyang, China.
Shu GuanDepartment of Surgical Oncology and Breast Surgery, The First Hospital of China Medical University, Shenyang, China.
Siqi WangDepartment of Radiation Oncology, The First Hospital of China Medical University, Shenyang, China.
Zhongxue YuDepartment of Cardiovascular Ultrasound, The First Hospital of China Medical University, Shenyang, China.
Tiancong LiuDepartment of Otolaryngology, Shengjing Hospital of China Medical University, Shenyang, China.
Shaonan DuDepartment of Neurosurgery, Shengjing Hospital of China Medical University, Shenyang, China.
Chen ZhuDepartment of Neurosurgery, The First Hospital of China Medical University, Shenyang, China.
China Medical University · CNFirst Hospital of China Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

aimMitochondria is one of the important organelles involved in cell energy metabolism and regulation and also play a key regulatory role in abnormal cell processes such as cell stress, cell damage, and cell canceration. Recent studies have shown that mitochondria can be transferred between cells in different ways and participate in the occurrence and development of many central nervous system diseases. We aim to review the mechanism of mitochondrial transfer in the progress of central nervous system diseases and the possibility of targeted therapy.

methodsThe PubMed databank, the China National Knowledge Infrastructure databank, and Wanfang Data were searched to identify the experiments of intracellular mitochondrial transferrin central nervous system. The focus is on the donors, receptors, transfer pathways, and targeted drugs of mitochondrial transfer.

resultsIn the central nervous system, neurons, glial cells, immune cells, and tumor cells can transfer mitochondria to each other. Meanwhile, there are many types of mitochondrial transfer, including tunneling nanotubes, extracellular vesicles, receptor cell endocytosis, gap junction channels, and intercellular contact. A variety of stress signals, such as the release of damaged mitochondria, mitochondrial DNA, or other mitochondrial products and the elevation of reactive oxygen species, can trigger the transfer of mitochondria from donor cells to recipient cells. Concurrently, a variety of molecular pathways and related inhibitors can affect mitochondrial intercellular transfer.

conclusionThis study reviews the phenomenon of intercellular mitochondrial transfer in the central nervous system and summarizes the corresponding transfer pathways. Finally, we propose targeted pathways and treatment methods that may be used to regulate mitochondrial transfer for the treatment of related diseases.

Indexed as

Central Nervous System DiseasesNanotubesBrainCell Membrane StructuresHumansMitochondriaTunneling Nanotubescentral nervous systemmitochondrial transfertargeted therapy

Identifiers

PMID37424172
PMCPMC10580346
OpenAlexW4383695453

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.