Evidence map›Paper›PMID 33437038›Full record

ArticleScientific reports2021

Aberrant spinal mechanical loading stress triggers intervertebral disc degeneration by inducing pyroptosis and nerve ingrowth.

Fangda Fu, Ronghua Bao, Sai Yao, Chengcong Zhou, Huan Luo, Zhiguo Zhang, Huihao Zhang, Yan Li, Shuxin Yan, Huan Yu and 9 more

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Scientific reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 63 papers.

0numbers the graph read from it
0cells of the map it votes in
63citing papers in PubMed
6.7field-weighted citation impact, top 2% 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

63 citing papers in PubMed, 73 citations in OpenAlex.

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  18. DDRGK1 preserves intervertebral disc development through ufmylation.Cellular and molecular life sciences : CMLS · 2025
    Article
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3 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

19 authors at 5 institutions in 1 country.

Fangda FuInstitute of Orthopaedics and Traumatology, the First Affiliated Hospital of Zhejiang Chinese Medical University, Hangzhou, 310053, Zhejiang, China.
Ronghua BaoHangzhou Fuyang Hospital of TCM Orthopedics and Traumatology, Hangzhou, 311400, Zhejiang, China.
Sai YaoInstitute of Orthopaedics and Traumatology, the First Affiliated Hospital of Zhejiang Chinese Medical University, Hangzhou, 310053, Zhejiang, China.
Chengcong ZhouInstitute of Orthopaedics and Traumatology, the First Affiliated Hospital of Zhejiang Chinese Medical University, Hangzhou, 310053, Zhejiang, China.
Huan LuoDepartment of Pharmacy, the Second Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, 310009, Zhejiang, China.
Zhiguo ZhangInstitute of Orthopaedics and Traumatology, the First Affiliated Hospital of Zhejiang Chinese Medical University, Hangzhou, 310053, Zhejiang, China.
Huihao ZhangInstitute of Orthopaedics and Traumatology, the First Affiliated Hospital of Zhejiang Chinese Medical University, Hangzhou, 310053, Zhejiang, China.
Yan LiThe First Clinical College, Zhejiang Chinese Medical University, Hangzhou, 310051, Zhejiang, China.
Shuxin YanThe First Clinical College, Zhejiang Chinese Medical University, Hangzhou, 310051, Zhejiang, China.
Huan YuInstitute of Orthopaedics and Traumatology, the First Affiliated Hospital of Zhejiang Chinese Medical University, Hangzhou, 310053, Zhejiang, China.
Weibin DuResearch Institute of Orthopedics, the Affiliated JiangNan Hospital of Zhejiang Chinese Medical University, Hangzhou, 311200, Zhejiang, China.
Yanping YangLonghua Hospital, Affiliated to Shanghai University of Traditional Chinese Medicine, Shanghai, 200032, China.
Hongting JinInstitute of Orthopaedics and Traumatology, the First Affiliated Hospital of Zhejiang Chinese Medical University, Hangzhou, 310053, Zhejiang, China.
Peijian TongInstitute of Orthopaedics and Traumatology, the First Affiliated Hospital of Zhejiang Chinese Medical University, Hangzhou, 310053, Zhejiang, China.
Zhi-Tao SunDepartment of Orthopedics, Shenzhen Traditional Chinese Hospital, Guangzhou University of Chinese Medicine, Shenzhen, 518055, China.
Ming YueDepartment of Physiology, Zhejiang Chinese Medical University, Hangzhou, 310053, China.
Di ChenResearch Center for Human Tissues and Organs Degeneration, Shenzhen Institutes of Advanced Technology, Chinese Academy of Sciences, Shenzhen, 518055, China.
Chengliang WuInstitute of Orthopaedics and Traumatology, the First Affiliated Hospital of Zhejiang Chinese Medical University, Hangzhou, 310053, Zhejiang, China. wcl@zcmu.edu.cn.
Hongfeng RuanInstitute of Orthopaedics and Traumatology, the First Affiliated Hospital of Zhejiang Chinese Medical University, Hangzhou, 310053, Zhejiang, China. rhf@zcmu.edu.cn.
Zhejiang Chinese Medical University · CNLonghua Hospital Shanghai University of Traditional Chinese Medicine · CNChinese Academy of Sciences · CNGuangzhou University of Chinese Medicine · CNSecond Affiliated Hospital of Zhejiang University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Aberrant mechanical factor is one of the etiologies of the intervertebral disc (IVD) degeneration (IVDD). However, the exact molecular mechanism of spinal mechanical loading stress-induced IVDD has yet to be elucidated due to a lack of an ideal and stable IVDD animal model. The present study aimed to establish a stable IVDD mouse model and evaluated the effect of aberrant spinal mechanical loading on the pathogenesis of IVDD. Eight-week-old male mice were treated with lumbar spine instability (LSI) surgery to induce IVDD. The progression of IVDD was evaluated by μCT and Safranin O/Fast green staining analysis. The metabolism of extracellular matrix, ingrowth of sensory nerves, pyroptosis in IVDs tissues were determined by immunohistological or real-time PCR analysis. The apoptosis of IVD cells was tested by TUNEL assay. IVDD modeling was successfully produced by LSI surgery, with substantial reductions in IVD height, BS/TV, Tb.N. and lower IVD score. LSI administration led to the histologic change of disc degeneration, disruption of the matrix metabolism, promotion of apoptosis of IVD cells and invasion of sensory nerves into annulus fibrosus, as well as induction of pyroptosis. Moreover, LSI surgery activated Wnt signaling in IVD tissues. Mechanical instability caused by LSI surgery accelerates the disc matrix degradation, nerve invasion, pyroptosis, and eventually lead to IVDD, which provided an alternative mouse IVDD model.

Indexed as

Wnt Signaling PathwayAnimalsDisease Models, AnimalExtracellular MatrixIntervertebral Disc DegenerationLumbar VertebraeMaleMiceMice, Inbred C57BLPyroptosisSensory Receptor CellsStress, Mechanical

Identifiers

PMID33437038
PMCPMC7804398
OpenAlexW3118272565

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.