Evidence map›Paper›PMID 34234890›Full record

ArticleAnimal cells and systems2021

MCT2 overexpression promotes recovery of cognitive function by increasing mitochondrial biogenesis in a rat model of stroke.

Xiaorong Yu, Rui Zhang, Cunsheng Wei, Yuanyuan Gao, Yanhua Yu, Lin Wang, Junying Jiang, Xuemei Zhang, Junrong Li, Xuemei Chen

Open access · goldAbstract read
In one paragraph

Article in Animal cells and systems, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.1field-weighted citation impact, top 23% 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

14 citing papers in PubMed, 19 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 2 institutions in 1 country.

Xiaorong YuDepartment of Neurology, The Affiliated Jiangning Hospital with Nanjing Medical University, Nanjing, People's Republic of China.
Rui ZhangDepartment of Neurology, The Affiliated Jiangning Hospital with Nanjing Medical University, Nanjing, People's Republic of China.
Cunsheng WeiDepartment of Neurology, The Affiliated Jiangning Hospital with Nanjing Medical University, Nanjing, People's Republic of China.
Yuanyuan GaoDepartment of General Practice, The Affiliated Jiangning Hospital with Nanjing Medical University, Nanjing, People's Republic of China.
Yanhua YuDepartment of Neurology, The Affiliated Jiangning Hospital with Nanjing Medical University, Nanjing, People's Republic of China.
Lin WangDepartment of Neurology, The Affiliated Jiangning Hospital with Nanjing Medical University, Nanjing, People's Republic of China.
Junying JiangDepartment of Neurology, The Affiliated Jiangning Hospital with Nanjing Medical University, Nanjing, People's Republic of China.
Xuemei ZhangDepartment of Neurology, The Affiliated Jiangning Hospital with Nanjing Medical University, Nanjing, People's Republic of China.
Junrong LiDepartment of Neurology, The Affiliated Jiangning Hospital with Nanjing Medical University, Nanjing, People's Republic of China.
Xuemei ChenDepartment of Neurology, The Affiliated Jiangning Hospital with Nanjing Medical University, Nanjing, People's Republic of China.
Nanjing Medical University · CNNanjing Jiangning Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Monocarboxylate transporter 2 (MCT2) is the predominant monocarboxylate transporter expressed by neurons. MCT2 plays an important role in brain energy metabolism. Stroke survivors are at high risk of cognitive impairment. We reported previously that stroke-induced cognitive impairment was related to impaired energy metabolism. In the present study, we report that cognitive function was impaired after stroke in rats. We found that MCT2 expression, but not that of MCT1 or MCT4, was markedly decreased in the rat hippocampus at 7 and 28 days after transient middle cerebral artery occlusion (tMCAO). Moreover, MCT2 overexpression promoted recovery of cognitive function after stroke. The molecular mechanism underlying these effects may be related to an increase in adenosine monophosphate-activated protein kinase-mediated mitochondrial biogenesis induced by overexpression of MCT2. Our findings suggest that MCT2 activation ameliorates cognitive impairment after stroke.

Indexed as

cognitive impairmentMCT2mitochondrial biogenesisStroke

Identifiers

PMID34234890
PMCPMC8118516
OpenAlexW3162334196

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.