Evidence map›Paper›PMID 34413501›Full record

ArticleGene therapy2022

CCR1 enhances SUMOylation of DGCR8 by up-regulating ERK phosphorylation to promote spinal nerve ligation-induced neuropathic pain.

Cunxian Shi, Jin Jin, Hongyu Xu, Jiahai Ma, Tao Li, Yonggang Xie, Zhen Li

Abstract read
PubMed Publisher
In one paragraph

Article in Gene therapy, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
1.0field-weighted citation impact, top 26% 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

11 citing papers in PubMed, 10 citations in OpenAlex.

  1. Article
  2. Electroacupuncture alleviates Parkinson's disease-related pain by inhibiting microglial NLRP3-ASC inflammasome in the amygdala.Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologicas · 2026
    Article
  3. Article
  4. Article
  5. Review
  6. Article
  7. Review
  8. Article
  9. Review
  10. Article
  11. SUMOylation and Major Depressive Disorder.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 3 institutions in 1 country.

Cunxian Shi *Department of Anesthesiology, The Affiliated Yantai Yuhuangding Hospital of Qingdao University, Yantai, China.
Jin Jin *Department of Anesthesiology, The Affiliated Yantai Yuhuangding Hospital of Qingdao University, Yantai, China.
Hongyu XuDepartment of Anesthesiology, Central Hospital of Zibo City, Zibo, China.
Jiahai MaDepartment of Anesthesiology, The Affiliated Yantai Yuhuangding Hospital of Qingdao University, Yantai, China.
Tao LiDepartment of Anesthesiology, The Affiliated Yantai Yuhuangding Hospital of Qingdao University, Yantai, China.
Yonggang XieDepartment of Anesthesiology, The Affiliated Yantai Yuhuangding Hospital of Qingdao University, Yantai, China. xyglzxrx@163.com.ORCID http://orcid.org/0000-0001-6065-9075
Zhen LiDepartment of Otorhinolaryngology, Yantaishan Hospital, Yantai, China. zhenlizb20@163.com.
Qingdao University · CNCentral Hospital of Zibo · CNYantaishan Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Neuropathic pain is a somatosensory nervous system dysfunction that remains a threatening health problem globally. Recent studies have highlighted the involvement of C-C motif chemokine receptor 1 (CCR1) in neuropathic pain. Herein, the current study set out to explore the modulatory role of CCR1 in spinal nerve ligation (SNL)-induced neuropathic pain and its underlying molecular mechanism. First, it was found that CCR1 was highly expressed in spinal cord tissues and microglial cells of SNL rats. On the other hand, CCR1 knockdown attenuated nerve pain in SNL rats and repressed microglial cell activation in SNL rats and also in the LPS-induced microglial cell model of nerve injury, as evidenced by elevated microglial cell markers OX-42 and IL-1β, IL-6 and TNF-α. Mechanistically, CCR1 enhanced small ubiquitin-like modifier 1 (SUMO1) modification of DiGeorge syndrome critical region gene 8 (DGCR8) in LPS-treated microglial cells by phosphorylating ERK. Moreover, CCR1 silencing brought about elevations in mechanical withdrawal threshold and thermal withdrawal latency. To conclude, our findings indicated that CCR1 enhanced the modification of DGCR8 by SUMO1 through phosphorylation of ERK, thereby promoting the activation and inflammatory response of spinal cord microglial cells and increasing the sensitivity of SNL rats to pain. Thus, this study offers a promising therapeutic target for the management of neuropathic pain.

Indexed as

NeuralgiaReceptors, ChemokineRNA-Binding ProteinsAnimalsDisease Models, AnimalExtracellular Signal-Regulated MAP KinasesLipopolysaccharidesPhosphorylationRatsRats, Sprague-DawleyReceptors, CCR1Spinal CordSpinal NervesSumoylationCcr1 protein, ratExtracellular Signal-Regulated MAP KinasesLipopolysaccharidesReceptors, CCR1Receptors, ChemokineRNA-Binding Proteins

Identifiers

PMID34413501
OpenAlexW3195321824

What OpenQuestion holds

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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.