Evidence map›Paper›PMID 37740187›Full record

ArticleMolecular medicine (Cambridge, Mass.)2023

Aerobic exercise improves cognitive impairment in mice with type 2 diabetes by regulating the MALAT1/miR-382-3p/BDNF signaling pathway in serum-exosomes.

Mingzhu Wang, Kangling Xie, Shengnan Zhao, Nan Jia, Yujiao Zong, Wenping Gu, Ying Cai

Open access · goldAbstract read
In one paragraph

Article in Molecular medicine (Cambridge, Mass.), 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed, 4 pooled it
4.9field-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

27 citing papers in PubMed, 4 syntheses or guidelines pooled it, 32 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

7 authors at 1 institution in 1 country.

Mingzhu Wang *National Clinical Research Center for Geriatric Disorders, Department of Rehabilitation, Xiangya Hospital Central South University, Changsha, 410008, Hunan, China.
Kangling Xie *National Clinical Research Center for Geriatric Disorders, Department of Rehabilitation, Xiangya Hospital Central South University, Changsha, 410008, Hunan, China.
Shengnan ZhaoNational Clinical Research Center for Geriatric Disorders, Department of Rehabilitation, Xiangya Hospital Central South University, Changsha, 410008, Hunan, China.
Nan JiaNational Clinical Research Center for Geriatric Disorders, Department of Rehabilitation, Xiangya Hospital Central South University, Changsha, 410008, Hunan, China.
Yujiao ZongNational Clinical Research Center for Geriatric Disorders, Department of Rehabilitation, Xiangya Hospital Central South University, Changsha, 410008, Hunan, China.
Wenping GuNational Clinical Research Center for Geriatric Disorders, Department of Neurology, Xiangya Hospital Central South University, Changsha, 410008, China.
Ying CaiNational Clinical Research Center for Geriatric Disorders, Department of Rehabilitation, Xiangya Hospital Central South University, Changsha, 410008, Hunan, China. 403991@csu.edu.cn.ORCID http://orcid.org/0000-0002-6284-8416
Central South University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundIt has been documented that aerobic exercise (AE) has a positive effect on improving cognitive function in type 2 diabetes (T2DM) patients. Here, we tried to explore how AE regulates the expression of long non-coding RNA in serum-exosomes (Exos), thereby affecting cognitive impairment in T2DM mice as well as its potential molecular mechanism.

methodsT2DM mouse models were constructed, and serum-Exos were isolated for whole transcriptome sequencing to screen differentially expressed lncRNA and mRNA, followed by prediction of downstream target genes. The binding ability of miR-382-3p with a long non-coding RNA MALAT1 and brain-derived neurotrophic factor (BDNF) was explored. Then, primary mouse hippocampal neurons were collected for in vitro mechanism verification, as evidenced by the detection of hippocampal neurons' vitality, proliferation, and apoptosis capabilities, and insulin resistance. Finally, in vivo mechanism verification was performed to assess the effect of AE on insulin resistance and cognitive disorder.

resultsTranscriptome sequencing analysis showed that MALAT1 was lowly expressed and miR-382-3p was highly expressed in serum-Exos samples of T2DM mice. There were targeted binding sites between MALAT1 and miR-382-3p and between miR-382-3p and BDNF. In vitro experiments showed that MALAT1 upregulated BDNF expression by inhibiting miR-382-3p. Silencing MALAT1 or overexpressing miR-382-3p could reduce the expression of INSR, IRS-1, IRS-2, PI3K/AKT, and Ras/MAPK, inhibit neuronal proliferation, and promote apoptosis. In vivo experiments further confirmed that AE could increase the expression of MALAT1 in serum-Exos to competitively inhibit miR-382-3p and upregulate BDNF expression, thereby improving cognitive impairment in T2DM mice.

conclusionAE may upregulate the expression of MALAT1 in serum-Exos to competitively inhibit miR-382-3p and upregulate BDNF expression, thus improving cognitive impairment in T2DM mice.

Indexed as

Cognitive DysfunctionDiabetes Mellitus, Type 2ExosomesInsulin ResistanceMicroRNAsRNA, Long NoncodingAnimalsBrain-Derived Neurotrophic FactorMicePhosphatidylinositol 3-KinasesSignal TransductionBdnf protein, mouseBrain-Derived Neurotrophic FactorMalat1 long non-coding RNA, mousemicroRNA 382, mouseMicroRNAsPhosphatidylinositol 3-KinasesRNA, Long NoncodingAerobic exerciseBDNFHippocampal neuronsMALAT1miR-382-3pNon-coding RNASerum-exosomesType 2 diabetes

Identifiers

PMID37740187
PMCPMC10517522
OpenAlexW4386968029

What Socratic 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 Socratic graph.