Evidence map›Paper›PMID 29436629›Full record

ArticleInternational journal of molecular medicine2018

Cognitive improvement following ischemia/reperfusion injury induced by voluntary running‑wheel exercise is associated with LncMALAT1‑mediated apoptosis inhibition.

Jin-Lin Shang, Qing Cheng, Sheng-Jie Duan, Lu Li, Li-Ya Jia

Open access · hybridAbstract read
In one paragraph

Article in International journal of molecular medicine, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
1.5field-weighted citation impact, top 20% 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

18 citing papers in PubMed, 32 citations in OpenAlex.

  1. Long non-coding RNAs in exercise: the hidden regulators of adaptation.Pflugers Archiv : European journal of physiology · 2026
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  6. Biomedical reports · 2024
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  15. Effects of precondition αNaunyn-Schmiedeberg's archives of pharmacology · 2020
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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

5 authors at 1 institution in 1 country.

Jin-Lin ShangNeurology Department, Heji Hospital Affiliated to Changzhi Medical College, Changzhi, Shaanxi 046011, P.R. China.
Qing ChengGeriatrics Department, Changzhi People Hospital, Changzhi, Shaanxi 046011, P.R. China.
Sheng-Jie DuanNeurology Department, Heji Hospital Affiliated to Changzhi Medical College, Changzhi, Shaanxi 046011, P.R. China.
Lu LiNeurology Department, Heji Hospital Affiliated to Changzhi Medical College, Changzhi, Shaanxi 046011, P.R. China.
Li-Ya JiaNeurology Department, Heji Hospital Affiliated to Changzhi Medical College, Changzhi, Shaanxi 046011, P.R. China.
Changzhi Medical College · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Previous human and animal studies demonstrated that voluntary exercise may improve cognitive function and facilitate neuronal plasticity in ischemia/reperfusion (I/R) models. However, the possible underlying mechanisms remain to be elucidated. Metastasis‑associated lung adenocarcinoma transcript 1 (MALAT1), a long noncoding RNA (lncRNA), may be associated with the functions and dysfunctions of endothelial cells. The present study investigated whether spontaneous running‑wheel (RW) exercise‑induced MALAT1 expression changes may be associated with the cognitive improvement of mice following I/R injury. The expression of MALAT1 was evaluated using reverse transcription‑quantitative polymerase chain reaction. Artificial MALAT1 and MALAT1 lentiviral mall interfering (siRNA) were used to alter MALAT1 expression levels in vivo. The Morris Water Maze test was performed to evaluate spatial learning and memory retention in the mice. Changes in the apoptotic rates of hippocampal neurons and levels of apoptosis‑associated proteins were also detected. The data revealed that MALAT1 increased in the hippocampus of mice in the RW‑treated I/R group and that this was associated with neurological, learning and memory improvement, reduced infarction volumes, decreased apoptosis and alterations to expression levels of apoptosis‑associated proteins. Following RW training in I/R‑injured mice, lentiviral MALAT1 siRNA conduction partially attenuated the protections induced by voluntary RW. However, exogenous MALAT1 treatment increased the protection. The current findings suggested that voluntary RW protected hippocampal neurons from I/R injury and promoted cognitive restoration, which was associated with lncRNA MALAT1‑mediated apoptosis inhibition.

Indexed as

ApoptosisCognitionExercise TherapyAnimalsBrainGene ExpressionHippocampusMaleMemoryMice, Inbred C57BLNeuronsReperfusion InjuryRNA, Long NoncodingRunningSpatial LearningMalat1 long non-coding RNA, mouseRNA, Long Noncoding

Identifiers

PMID29436629
PMCPMC5846661
OpenAlexW2793447330

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.