Evidence map›Paper›PMID 35606793›Full record

ArticleArthritis research & therapy2022

Excessive mechanical stress-induced intervertebral disc degeneration is related to Piezo1 overexpression triggering the imbalance of autophagy/apoptosis in human nucleus pulpous.

Sheng Shi, Xing-Jian Kang, Zhi Zhou, Zhi-Min He, Shuang Zheng, Shi-Sheng He

Open access · goldAbstract read
In one paragraph

Article in Arthritis research & therapy, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 76 papers.

0numbers the graph read from it
0cells of the map it votes in
76citing papers in PubMed
12.2field-weighted citation impact, top 1% 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

76 citing papers in PubMed, 88 citations in OpenAlex.

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16 more citing papers are in PubMed but not listed here.

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

6 authors at 4 institutions in 1 country.

Sheng ShiDepartment of Orthopaedics, Shanghai Tenth People's Hospital, Tongji University, Shanghai, 200072, People's Republic of China.
Xing-Jian KangSchool of Stomatology, Wenzhou Medical University, Wenzhou, 325000, People's Republic of China.
Zhi ZhouDepartment of Orthopaedics, Shanghai Tenth People's Hospital, Tongji University, Shanghai, 200072, People's Republic of China.
Zhi-Min HeDepartment of Orthopaedics, Shanghai Tenth People's Hospital, Tongji University, Shanghai, 200072, People's Republic of China.
Shuang ZhengSchool of Medicine, Shanghai University, Shanghai, 200444, People's Republic of China. 75548043@qq.com.
Shi-Sheng HeDepartment of Orthopaedics, Shanghai Tenth People's Hospital, Tongji University, Shanghai, 200072, People's Republic of China. 309834056@qq.com.
Shanghai Tenth People's Hospital · CNTongji University · CNShanghai University · CNWenzhou Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundMechanical stress plays a crucial role in the pathogenesis of intervertebral disc degeneration (IVDD). The mechanosensitive Piezo1 ion channel can sense the changes in mechanical stress and convert the mechanical signals into chemical signals. This study aims to investigate the effect of Piezo1 on the mechanical stress-induced IVDD and explore the possible mechanism.

methodsThe expression of Piezo1 and collagen II in immunohistochemical staining, cervical curvature, and the stiffness of nucleus pulpous (NP) were performed in normal and degenerated human intervertebral discs. In the experiment, high-intensity compression was applied to mimic the mechanical environment of IVDD. The cell viability, matrix macromolecules, and pro-inflammatory cytokines were examined to investigate the effect of Piezo1 on mechanical stress-treated NP cells. Additionally, autophagy condition of NP cells was detected within high-intensity compression and/or the inhibitor of Piezo1, GsMTx4.

resultsThe up-expression of Piezo1, down-expression of Col II, elevated stiffness of NP, and poor kyphosis were observed in degenerated human intervertebral discs. High-intensity stress significantly decreased cell viability and the synthesis of extracellular matrix but increased the expression of senescence-associated proteins (p53 and p16) and pro-inflammatory cytokines (TNF-α, IL-6 and IL-1β) by mitochondrial dysfunction and suppression of autophagy. However, GsMTx4 can partly attenuate these effects.

conclusionPiezo1 upregulation under excessive mechanical stress promotes the apoptosis, senescence, and pro-inflammatory cytokines of NP and leads to the loss of extracellular matrix by mitochondrial dysfunction and the suppression of autophagy; on the other hand, the inhibition of Piezo1 can partly alleviate these effects.

Indexed as

Intervertebral Disc DegenerationIon ChannelsNucleus PulposusApoptosisAutophagyCytokinesHumansStress, MechanicalCytokinesIon ChannelsPIEZO1 protein, humanAutophagyIntervertebral disc degenerationMechanical stressNucleus pulpousPiezo 1

Identifiers

PMID35606793
PMCPMC9125856
OpenAlexW4281296177

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.