Evidence map›Paper›PMID 33156817›Full record

ReviewMedical science monitor : international medical journal of experimental and clinical research2020

Mitochondrial Fusion and Fission in Neuronal Death Induced by Cerebral Ischemia-Reperfusion and Its Clinical Application: A Mini-Review.

Yike Chen, Songxue Guo, Yajuan Tang, Chaohui Mou, Xinben Hu, Fangjie Shao, Wei Yan, Qun Wu

Open access · greenAbstract readReview
In one paragraph

Review in Medical science monitor : international medical journal of experimental and clinical research, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
1.8field-weighted citation impact, top 14% 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

22 citing papers in PubMed, 36 citations in OpenAlex.

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  3. Ferroptosis in depression: mechanisms, association, and therapeutic strategies.Journal of neural transmission (Vienna, Austria : 1996) · 2026
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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

8 authors at 2 institutions in 1 country.

Yike ChenDepartment of Neurosurgery, Second Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou, Zhejiang, China (mainland).
Songxue GuoDepartment of Plastic Surgery, Second Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou, Zhejiang, China (mainland).
Yajuan TangDepartment of Neurosurgery, Second Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou, Zhejiang, China (mainland).
Chaohui MouDepartment of Neurosurgery, Taizhou First People's Hospital, Taizhou, Zhejiang, China (mainland).
Xinben HuDepartment of Neurosurgery, Second Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou, Zhejiang, China (mainland).
Fangjie ShaoDepartment of Neurosurgery, Second Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou, Zhejiang, China (mainland).
Wei YanDepartment of Neurosurgery, Second Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou, Zhejiang, China (mainland).
Qun WuDepartment of Neurosurgery, Second Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou, Zhejiang, China (mainland).
Second Affiliated Hospital of Zhejiang University · CNTaizhou First People's Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Mitochondria are highly dynamic organelles which are joined by mitochondrial fusion and divided by mitochondrial fission. The balance of mitochondrial fusion and fission plays a critical role in maintaining the normal function of neurons, of which the processes are both mediated by several proteins activated by external stimulation. Cerebral ischemia-reperfusion (I/R) injury can disrupt the balance of mitochondrial fusion and fission through regulating the expression and post-translation modification of fusion- and fission-related proteins, thereby destroying homeostasis of the intracellular environment and causing neuronal death. Furthermore, human intervention in fusion- and fission-related proteins can influence the function of neurons and change the outcomes of cerebral I/R injury. In recent years, researchers have found that mitochondrial dysfunction was one of the main factors involved in I/R, and mitochondria is an attractive target in I/R neuroprotection. Therefore, mitochondrial-targeted therapy of the nervous system for I/R gradually started from basic study to clinical application. In the present review, we highlight recent progress in mitochondria fusion and fission in neuronal death induced by cerebral I/R to help understanding the regulatory factors and signaling networks of aberrant mitochondrial fusion and fission contributing to neuronal death during I/R, as well as the potential neuroprotective therapeutics targeting mitochondrial dynamics, which may help clinical treatment and development of relevant dugs.

Indexed as

Mitochondrial DynamicsAnimalsAutophagyBrain IschemiaCell DeathHumansNeuronsReperfusion Injury

Identifiers

PMID33156817
PMCPMC7654336
OpenAlexW3095060673

What OpenQuestion 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 OpenQuestion graph.