Evidence map›Paper›PMID 36074556›Full record

ArticleCNS neuroscience & therapeutics2022

Sam50 exerts neuroprotection by maintaining the mitochondrial structure during experimental cerebral ischemia/reperfusion injury in rats.

Xulong Yin, Jiahe Wang, Siyuan Yang, Haiying Li, Haitao Shen, Hui Wang, Xiang Li, Gang Chen

Open access · goldAbstract read
In one paragraph

Article in CNS neuroscience & therapeutics, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
0.7field-weighted citation impact, top 33% 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

9 citing papers in PubMed, 9 citations in OpenAlex.

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  8. Ablation ofbioRxiv : the preprint server for biology · 2023
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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 1 institution in 1 country.

Xulong YinDepartment of Neurology, The First Affiliated Hospital of Soochow University, Suzhou, China.
Jiahe WangInstitute of Stroke Research, Soochow University, Suzhou, China.
Siyuan YangInstitute of Stroke Research, Soochow University, Suzhou, China.
Haiying LiInstitute of Stroke Research, Soochow University, Suzhou, China.
Haitao ShenInstitute of Stroke Research, Soochow University, Suzhou, China.ORCID 0000-0001-9296-3725
Hui WangDepartment of Neurology, The First Affiliated Hospital of Soochow University, Suzhou, China.
Xiang LiInstitute of Stroke Research, Soochow University, Suzhou, China.ORCID 0000-0002-9918-5847
Gang ChenInstitute of Stroke Research, Soochow University, Suzhou, China.ORCID 0000-0002-0758-1907
Soochow University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

aimTo investigate the role of Sam50, a barrel protein on the surface of the mitochondrial outer membrane, in cerebral ischemia-reperfusion (I/R) injury and its underlying mechanisms.

methodsA middle cerebral artery occlusion/reperfusion (MCAO/R) model in adult male Sprague-Dawley rats was established in vivo, and cultured neurons were exposed to oxygen-glucose deprivation/reoxygenation (OGD/R) to simulate I/R injury in vitro. Lentiviral vector encoding Sam50 or Sam50 shRNA was constructed and administered to rats by intracerebroventricular injection to overexpress and knockdown Sam50, respectively.

resultsFirst, after MCAO/R induction, the mitochondrial structure was damaged, and Sam50 protein levels were increased responsively both in vivo and in vitro. Then, it was found that Sam50 overexpression could reduce infarction size, inhibit neuronal cell death, improve neurobehavioral disability, protect mitochondrial structure integrity, and ameliorate mitochondrial dysfunction, which was induced by I/R injury both in vivo and in vitro. However, Sam50 downregulation showed the opposite results and aggravated I/R injury by inducing neuronal cell death, neurobehavioral disability, and mitochondrial dysfunction. Moreover, we found that the interaction between Sam50 and Mic19 was broken off after OGD/R, showing that the Sam50-Mic19-Mic60 axis was breakage in neurons, which would be a reason for mitochondrial structure and function abnormalities induced by I/R injury.

conclusionSam50 played a vital role in the protection of neurons and mitochondria in cerebral I/R injury, which could be a novel target for mitochondrial protection and ameliorating I/R injury.

Indexed as

Brain IschemiaReperfusion InjuryAnimalsInfarction, Middle Cerebral ArteryMaleMitochondriaNeuroprotectionRatsRats, Sprague-Dawleyischemia-reperfusion injurymitochondriaSam50Sam50-Mic19-Mic60 axis

Identifiers

PMID36074556
PMCPMC9627377
OpenAlexW4294958904

What OpenQuestion holds

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LicenceCC BY
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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.