Evidence map›Paper›PMID 29512682›Full record

ArticleInternational journal of molecular medicine2018

Cyclic mechanical tension reinforces DNA damage and activates the p53-p21-Rb pathway to induce premature senescence of nucleus pulposus cells.

Chencheng Feng, Minghui Yang, Yang Zhang, Minghong Lan, Bo Huang, Huan Liu, Yue Zhou

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 47 papers.

0numbers the graph read from it
0cells of the map it votes in
47citing papers in PubMed
3.7field-weighted citation impact, top 7% 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

47 citing papers in PubMed, 53 citations in OpenAlex.

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  12. Mechanical Stress Triggers Premature Senescence in Cardiac Fibroblasts.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025
    Article
  13. The Effects of Vertebral Body Tethering on the Intervertebral Discs and Facet Joints: A Numerical Analysis.International journal for numerical methods in biomedical engineering · 2025
    Article
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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

7 authors at 2 institutions in 1 country.

Chencheng FengDepartment of Orthopedics, Xinqiao Hospital, Third Military Medical University, Chongqing 400037, P.R. China.
Minghui YangDepartment of Orthopedics, Xinqiao Hospital, Third Military Medical University, Chongqing 400037, P.R. China.
Yang ZhangDepartment of Orthopedics, Xinqiao Hospital, Third Military Medical University, Chongqing 400037, P.R. China.
Minghong LanDepartment of Orthopedics, Xinqiao Hospital, Third Military Medical University, Chongqing 400037, P.R. China.
Bo HuangDepartment of Orthopedics, Xinqiao Hospital, Third Military Medical University, Chongqing 400037, P.R. China.
Huan LiuDepartment of Orthopedics, Xinqiao Hospital, Third Military Medical University, Chongqing 400037, P.R. China.
Yue ZhouDepartment of Orthopedics, Xinqiao Hospital, Third Military Medical University, Chongqing 400037, P.R. China.
Army Medical University · CNXinqiao Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Intervertebral disc (IVD) degeneration (IDD) is a widely recognized contributor to low back pain. Mechanical stress is a crucial etiological factor of IDD. During the process of IDD, a vicious circle is formed between abnormal mechanical stress and the damage of disc structure and function. Notably, the pathological process of IDD is mediated by the phenotypic shift of IVD cells from an extracellular matrix anabolic phenotype to a catabolic and pro-inflammatory phenotype. Therefore, the effects of mechanical stress on the initiation and progression of IDD depend on the mechanobiology of IVD cells. Recently, disc cell senescence was identified as a new hallmark of IDD. However, the senescent response of disc cells to mechanical stress remains unknown. In this study, we found that prolonged exposure of cyclic mechanical tension (CMT) with unphysiological magnitude generated by the Flexercell tension system markedly induced premature senescence of nucleus pulposus (NP) cells. CMT augmented the DNA damage of NP cells, but did not affect the redox homeostasis of NP cells. Moreover, the p53-p21-retinoblastoma protein (Rb) pathway was activated by CMT to mediate the CMT-induced premature senescence of NP cells. The findings are beneficial to understanding the mechanism of disc cell senescence and the mechanobiology of disc cells further. It suggests that prolonged abnormal mechanical stress accelerates the establishment and progression of disc cell senescence and consequently impairs the structural and functional homeostasis of IVDs to cause IDD. Preventing the pro-senescent effect of mechanical stress on IVD cells is a promising approach to delay the process of IDD.

Indexed as

AnimalsCellular SenescenceDNA DamageIntervertebral Disc DegenerationMaleNucleus PulposusRatsRats, Sprague-DawleyReactive Oxygen SpeciesStress, MechanicalTumor Suppressor Protein p53Reactive Oxygen SpeciesTumor Suppressor Protein p53

Identifiers

PMID29512682
PMCPMC5881642
OpenAlexW2792444892

What OpenQuestion holds

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LicenceCC BY-NC-ND
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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.