Evidence map›Paper›PMID 34849186›Full record

ArticleOxidative medicine and cellular longevity2021

Mitochondrial Transplantation Attenuates Cerebral Ischemia-Reperfusion Injury: Possible Involvement of Mitochondrial Component Separation.

Qiang Xie, Jun Zeng, Yongtao Zheng, Tianwen Li, Junwei Ren, Kezhu Chen, Quan Zhang, Rong Xie, Feng Xu, Jianhong Zhu

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

Article in Oxidative medicine and cellular longevity, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.

0numbers the graph read from it
0cells of the map it votes in
45citing papers in PubMed
4.2field-weighted citation impact, top 4% 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

45 citing papers in PubMed, 69 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

10 authors at 1 institution in 1 country.

Qiang XieFudan University Huashan Hospital, Department of Neurosurgery, National Center for Neurological Disorders, National Key Laboratory for Medical Neurobiology, Shanghai Key Laboratory of Brain Function and Regeneration, Institutes of Brain Science, MOE Frontiers Center for Brain Science, Shanghai Medical College-Fudan University, 12 Wulumuqi Zhong Rd., Shanghai 200040, China.ORCID https://orcid.org/0000-0003-0669-6021
Jun ZengFudan University Huashan Hospital, Department of Neurosurgery, National Center for Neurological Disorders, National Key Laboratory for Medical Neurobiology, Shanghai Key Laboratory of Brain Function and Regeneration, Institutes of Brain Science, MOE Frontiers Center for Brain Science, Shanghai Medical College-Fudan University, 12 Wulumuqi Zhong Rd., Shanghai 200040, China.ORCID https://orcid.org/0000-0002-8185-7940
Yongtao ZhengFudan University Huashan Hospital, Department of Neurosurgery, National Center for Neurological Disorders, National Key Laboratory for Medical Neurobiology, Shanghai Key Laboratory of Brain Function and Regeneration, Institutes of Brain Science, MOE Frontiers Center for Brain Science, Shanghai Medical College-Fudan University, 12 Wulumuqi Zhong Rd., Shanghai 200040, China.ORCID https://orcid.org/0000-0002-4590-8720
Tianwen LiFudan University Huashan Hospital, Department of Neurosurgery, National Center for Neurological Disorders, National Key Laboratory for Medical Neurobiology, Shanghai Key Laboratory of Brain Function and Regeneration, Institutes of Brain Science, MOE Frontiers Center for Brain Science, Shanghai Medical College-Fudan University, 12 Wulumuqi Zhong Rd., Shanghai 200040, China.ORCID https://orcid.org/0000-0002-6979-8220
Junwei RenFudan University Huashan Hospital, Department of Neurosurgery, National Center for Neurological Disorders, National Key Laboratory for Medical Neurobiology, Shanghai Key Laboratory of Brain Function and Regeneration, Institutes of Brain Science, MOE Frontiers Center for Brain Science, Shanghai Medical College-Fudan University, 12 Wulumuqi Zhong Rd., Shanghai 200040, China.ORCID https://orcid.org/0000-0001-9778-6975
Kezhu ChenFudan University Huashan Hospital, Department of Neurosurgery, National Center for Neurological Disorders, National Key Laboratory for Medical Neurobiology, Shanghai Key Laboratory of Brain Function and Regeneration, Institutes of Brain Science, MOE Frontiers Center for Brain Science, Shanghai Medical College-Fudan University, 12 Wulumuqi Zhong Rd., Shanghai 200040, China.ORCID https://orcid.org/0000-0001-9710-708X
Quan ZhangFudan University Huashan Hospital, Department of Neurosurgery, National Center for Neurological Disorders, National Key Laboratory for Medical Neurobiology, Shanghai Key Laboratory of Brain Function and Regeneration, Institutes of Brain Science, MOE Frontiers Center for Brain Science, Shanghai Medical College-Fudan University, 12 Wulumuqi Zhong Rd., Shanghai 200040, China.ORCID https://orcid.org/0000-0002-5656-1064
Rong XieFudan University Huashan Hospital, Department of Neurosurgery, National Center for Neurological Disorders, National Key Laboratory for Medical Neurobiology, Shanghai Key Laboratory of Brain Function and Regeneration, Institutes of Brain Science, MOE Frontiers Center for Brain Science, Shanghai Medical College-Fudan University, 12 Wulumuqi Zhong Rd., Shanghai 200040, China.ORCID https://orcid.org/0000-0002-8277-7280
Feng XuFudan University Huashan Hospital, Department of Neurosurgery, National Center for Neurological Disorders, National Key Laboratory for Medical Neurobiology, Shanghai Key Laboratory of Brain Function and Regeneration, Institutes of Brain Science, MOE Frontiers Center for Brain Science, Shanghai Medical College-Fudan University, 12 Wulumuqi Zhong Rd., Shanghai 200040, China.ORCID https://orcid.org/0000-0002-7976-4446
Jianhong ZhuFudan University Huashan Hospital, Department of Neurosurgery, National Center for Neurological Disorders, National Key Laboratory for Medical Neurobiology, Shanghai Key Laboratory of Brain Function and Regeneration, Institutes of Brain Science, MOE Frontiers Center for Brain Science, Shanghai Medical College-Fudan University, 12 Wulumuqi Zhong Rd., Shanghai 200040, China.ORCID https://orcid.org/0000-0001-9004-651X
Fudan University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundMitochondrial dysfunctions play a pivotal role in cerebral ischemia-reperfusion (I/R) injury. Although mitochondrial transplantation has been recently explored for the treatment of cerebral I/R injury, the underlying mechanisms and fate of transplanted mitochondria are still poorly understood.

methodsMitochondrial morphology and function were assessed by fluorescent staining, electron microscopy, JC-1, PCR, mitochondrial stress testing, and metabolomics. Therapeutic effects of mitochondria were evaluated by cell viability, reactive oxygen species (ROS), and apoptosis levels in a cellular hypoxia-reoxygenation model. Rat middle cerebral artery occlusion model was applied to assess the mitochondrial therapy in vivo. Transcriptomics was performed to explore the underlying mechanisms. Mitochondrial fate tracking was implemented by a variety of fluorescent labeling methods.

resultsNeuro-2a (N2a) cell-derived mitochondria had higher mitochondrial membrane potential, more active oxidative respiration capacity, and less mitochondrial DNA copy number. Exogenous mitochondrial transplantation increased cellular viability in an oxygen-dependent manner, decreased ROS and apoptosis levels, improved neurobehavioral deficits, and reduced infarct size. Transcriptomic data showed that the differential gene enrichment pathways are associated with metabolism, especially lipid metabolism. Mitochondrial tracking indicated specific parts of the exogenous mitochondria fused with the mitochondria of the host cell, and others were incorporated into lysosomes. This process occurred at the beginning of internalization and its efficiency is related to intercellular connection.

conclusionsMitochondrial transplantation may attenuate cerebral I/R injury. The mechanism may be related to mitochondrial component separation, altering cellular metabolism, reducing ROS, and apoptosis in an oxygen-dependent manner. The way of isolated mitochondrial transfer into the cell may be related to intercellular connection.

Indexed as

AnimalsBrain IschemiaMaleMitochondriaRatsRats, Sprague-DawleyReperfusion Injury

Identifiers

PMID34849186
PMCPMC8627565
OpenAlexW3217227550

What OpenQuestion holds

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LicenceCC BY
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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.