Evidence map›Paper›PMID 26647915›Full record

ArticleInternational journal of molecular medicine2016

Electroacupuncture protects against ischemic stroke by reducing autophagosome formation and inhibiting autophagy through the mTORC1-ULK1 complex-Beclin1 pathway.

Weilin Liu, Guanhao Shang, Shanli Yang, Jia Huang, Xiehua Xue, Yunjiao Lin, Yi Zheng, Xian Wang, Lulu Wang, Ruhui Lin and 2 more

Open access · hybridAbstract read
In one paragraph

Article in International journal of molecular medicine, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed
3.3field-weighted citation impact, top 8% 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

35 citing papers in PubMed, 61 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

12 authors at 1 institution in 1 country.

Weilin LiuCollege of Rehabilitation Medicine, Fujian University of Traditional Chinese Medicine, Fuzhou, Fujian 350122, P.R. China.
Guanhao ShangThe Fujian Province Key Laboratory of Motor Functional Rehabilitation, Fuzhou, Fujian 350001, P.R. China.
Shanli YangRehabilitation Hospital Affiliated to Fujian University of Traditional Chinese Medicine, Fuzhou, Fujian 350001, P.R. China.
Jia HuangCollege of Rehabilitation Medicine, Fujian University of Traditional Chinese Medicine, Fuzhou, Fujian 350122, P.R. China.
Xiehua XueRehabilitation Hospital Affiliated to Fujian University of Traditional Chinese Medicine, Fuzhou, Fujian 350001, P.R. China.
Yunjiao LinThe Fujian Province Key Laboratory of Motor Functional Rehabilitation, Fuzhou, Fujian 350001, P.R. China.
Yi ZhengThe Fujian Province Key Laboratory of Motor Functional Rehabilitation, Fuzhou, Fujian 350001, P.R. China.
Xian WangThe Fujian Province Key Laboratory of Motor Functional Rehabilitation, Fuzhou, Fujian 350001, P.R. China.
Lulu WangThe Fujian Province Key Laboratory of Motor Functional Rehabilitation, Fuzhou, Fujian 350001, P.R. China.
Ruhui LinThe Fujian Province Key Laboratory of Motor Functional Rehabilitation, Fuzhou, Fujian 350001, P.R. China.
Jing TaoCollege of Rehabilitation Medicine, Fujian University of Traditional Chinese Medicine, Fuzhou, Fujian 350122, P.R. China.
Lidian ChenCollege of Rehabilitation Medicine, Fujian University of Traditional Chinese Medicine, Fuzhou, Fujian 350122, P.R. China.
Fujian University of Traditional Chinese Medicine · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

In a previous study by our group, we demonstrated that electroacupuncture (EA) activates the class I phosphoinositide 3-kinase (PI3K)/Akt signaling pathway. There is considerable evidence that the downstream mammalian target of rapamycin complex 1 (mTORC1) plays an important role in autophagy following ischemic stroke. The aim of the present study was to determine whether EA exerts a neuroprotective effect through mTORC1-mediated autophagy following ischemia/reperfusion injury. Our results revealed that EA at the LI11 and ST36 acupoints attenuated motor dysfunction, improved neurological deficit outcomes and decreased the infarct volumes. The number of autophagosomes, autolysosomes and lysosomes was decreased following treatment with EA. Simultaneously, the levels of the autophagosome membrane maker, microtubule-associated protein 1 light chain 3 beta (LC3B)Ⅱ/Ⅰ, Unc-51-like kinase 1 (ULK1), autophagy related gene 13 Atg13) and Beclin1 (ser14) were decreased, whereas mTORC1 expression was increased in the peri-infarct cortex. These results suggest that EA protects against ischemic stroke through the inhibition of autophagosome formation and autophagy, which is mediated through the mTORC1-ULK complex-Beclin1 pathway.

Indexed as

Acupuncture PointsAnimalsApoptosis Regulatory ProteinsAutophagyAutophagy-Related Protein-1 HomologBeclin-1Disease Models, AnimalElectroacupunctureHumansIntracellular Signaling Peptides and ProteinsLysosomesMechanistic Target of Rapamycin Complex 1Multiprotein ComplexesNeuroprotective AgentsPhagosomesRatsApoptosis Regulatory ProteinsAutophagy-Related Protein-1 HomologBeclin-1Becn1 protein, ratIntracellular Signaling Peptides and ProteinsMechanistic Target of Rapamycin Complex 1Multiprotein ComplexesNeuroprotective AgentsTOR Serine-Threonine KinasesULK1 protein, rat

Identifiers

PMID26647915
PMCPMC4716798
OpenAlexW2190909122

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.