Evidence map›Paper›PMID 32945105›Full record

ArticleJournal of cellular and molecular medicine2020

Mechanical stress regulates autophagic flux to affect apoptosis after spinal cord injury.

Xin Zhang, Yingli Jing, Chuan Qin, Changbin Liu, Degang Yang, Feng Gao, Mingliang Yang, Liangjie Du, Jianjun Li

Open access · goldAbstract read
In one paragraph

Article in Journal of cellular and molecular medicine, 2020. 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
4.4field-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

18 citing papers in PubMed, 43 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

9 authors at 3 institutions in 1 country.

Xin ZhangSchool of Rehabilitation Medicine, Capital Medical University, Beijing, China.
Yingli JingChina Rehabilitation Science Institute, Beijing, China.
Chuan QinSchool of Rehabilitation Medicine, Capital Medical University, Beijing, China.
Changbin LiuDepartment of Rehabilitation Medicine, Beijing Tiantan Hospital, Beijing, China.
Degang YangSchool of Rehabilitation Medicine, Capital Medical University, Beijing, China.
Feng GaoSchool of Rehabilitation Medicine, Capital Medical University, Beijing, China.
Mingliang YangSchool of Rehabilitation Medicine, Capital Medical University, Beijing, China.
Liangjie DuSchool of Rehabilitation Medicine, Capital Medical University, Beijing, China.
Jianjun LiSchool of Rehabilitation Medicine, Capital Medical University, Beijing, China.ORCID 0000-0003-2663-5971
Capital Medical University · CNBeijing Tian Tan Hospital · CNChina Rehabilitation Research Center · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Increased mechanical stress after spinal cord injury (SCI) expands the scope of nerve tissue damage and exacerbates nerve function defects. Surgical decompression after SCI is a conventional therapeutic strategy and has been proven to have neuroprotective effects. However, the mechanisms of the interaction between mechanical stress and neurons are currently unknown. In this study, we monitored intramedullary pressure (IMP) and investigated the therapeutic benefit of decompression (including durotomy and piotomy) after injury and its underlying mechanisms in SCI. We found that decreased IMP promotes the generation and degradation of LC3 II, promotes the degradation of p62 and enhances autophagic flux to alleviate apoptosis. The lysosomal dysfunction was reduced after decompression. Piotomy was better than durotomy for the histological repair of spinal cord tissue after SCI. However, the autophagy-lysosomal pathway inhibitor chloroquine (CQ) partially reversed the apoptosis inhibition caused by piotomy after SCI, and the structural damage was also aggravated after CQ administration. An antibody microarray analysis showed that decompression may reverse the up-regulated abundance of p-PI3K, p-AKT and p-mTOR caused by SCI. Our findings may contribute to a better understanding of the mechanism of decompression and the effects of mechanical stress on autophagy after SCI.

Indexed as

ApoptosisAutophagyStress, MechanicalAnimalsChloroquineDecompression, SurgicalDisease Models, AnimalFemaleLysosomesPhosphatidylinositol 3-KinasesPhosphorylationProto-Oncogene Proteins c-aktRabbitsSpinal Cord InjuriesTOR Serine-Threonine KinasesUp-RegulationChloroquinePhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktTOR Serine-Threonine Kinasesapoptosisautophagic fluxdecompressionmechanical stressmTORspinal cord injury

Identifiers

PMID32945105
PMCPMC7686991
OpenAlexW3087203638

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.