Evidence map›Paper›PMID 35332432›Full record

ArticleHuman cell2022

UBR3 promotes inflammation and apoptosis via DUSP1/p38 pathway in the nucleus pulposus cells of patients with intervertebral disc degeneration.

Zhenhuan Jiang, Qinghua Zhao, Liang Chen, Yifeng Luo, Lei Shen, Zhihong Cao, Qiang Wang

Abstract read
PubMed Publisher
In one paragraph

Article in Human cell, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
2.1field-weighted citation impact, top 13% 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

13 citing papers in PubMed, 14 citations in OpenAlex.

  1. Review
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  6. Review
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  9. Gene polymorphisms ofJournal of Cancer · 2024
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  13. Role of the Intermediate Filament Protein Peripherin in Health and Disease.International journal of molecular sciences · 2022
    Review
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.

Zhenhuan Jiang *Department of Orthopaedics, The Affiliated Yixing Hospital of Jiangsu University, Yixing, China.
Qinghua Zhao *Department of Orthopaedics, School of Medicine, Shanghai First People's Hospital, Shanghai Jiaotong University, Shanghai, China.
Liang ChenDepartment of Orthopaedics, The Affiliated Yixing Hospital of Jiangsu University, Yixing, China.
Yifeng LuoDepartment of Radiology, The Affiliated Yixing Hospital of Jiangsu University, Yixing, China.
Lei ShenDepartment of Orthopaedics, The Affiliated Yixing Hospital of Jiangsu University, Yixing, China.
Zhihong CaoDepartment of Radiology, The Affiliated Yixing Hospital of Jiangsu University, Yixing, China. staff877@yxph.com.
Qiang WangDepartment of Orthopaedics, The Affiliated Yixing Hospital of Jiangsu University, Yixing, China. qiangwang258@163.com.ORCID http://orcid.org/0000-0001-9607-4650
Jiangsu University · CNShanghai First People's Hospital · CN

Funding

jiangsu health international exchange program of jiangsu commission of health JSH-2018-017scientific research project of jiangsu commission of health Z2020006
6 · The paper itself

Abstract

Intervertebral disc disease (IDD) is a primary cause of low back pain, affecting 5% of individuals. Previous study have shown that dual-specificity (Thr/Tyr) phosphatase 1 (DUSP1) regulates p38 MAPK activity and DUSP1 level is regulated by ubiquitination. As an E3 ubiquitin-protein ligase, UBR3 has been shown to regulate a variety of biological processes through ubiquitination. However, the role of UBR3/DUSP1/p38 in IDD remains to be elucidated. In the current study, we found that UBR3 was significantly increased in the nucleus pulposus tissues of IDD patients and was correlated with IDD severity. Silencing UBR3 promoted the growth, inhibited apoptosis, and inhibited inflammation in primary NPCs. Mechanism study suggested that UBR3 exerted its effects through p38. Co-immunoprecipitation assay indicated that UBR3 promoted DUSP1 ubiquitination. Overexpression of DUSP1 reversed the effect of UBR3 overexpression. Our data also supported that UBR3 was positively correlated with p-p38, but negatively correlated with DUSP1 in IDD. In summary, UBR3 promotes inflammation and apoptosis via inhibiting the p38 signaling pathway by DUSP1 ubiquitination in the NPCs of IDD patients. These findings highlight the importance of UBR3/DUSP1/p38 signaling pathway in IDD and provide new insights for the prevention and treatment of IDD.

Indexed as

Intervertebral Disc DegenerationNucleus PulposusApoptosisDual Specificity Phosphatase 1HumansInflammationIntervertebral Disc DisplacementDual Specificity Phosphatase 1DUSP1 protein, humanApoptosisInflammationIntervertebral disc degenerationNucleus pulposus cellsUbiquitination

Identifiers

PMID35332432
OpenAlexW4220665724

What OpenQuestion holds

Textmetadata
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.