Evidence map›Paper›PMID 37220667›Full record

ReviewMolecular pain

Inflammation in pathogenesis of chronic pain: Foe and friend.

Xiao-Xia Fang, Meng-Nan Zhai, Meixuan Zhu, Cheng He, Heng Wang, Juan Wang, Zhi-Jun Zhang

Open access · goldAbstract readReview
In one paragraph

Review in Molecular pain. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 76 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
76citing papers in PubMed, 2 pooled it
19.6field-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, 2 syntheses or guidelines pooled it, 112 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Article
  4. Review
  5. Article
  6. Review
  7. Betanin fromBiomedicines · 2026
    Article
  8. Review
  9. Review
  10. Review
  11. Article
  12. Chronic Pain and Cognitive Dysfunction: Clinical Implement, Mechanism, and Therapeutic Strategy.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2026
    Review
  13. Review
  14. Article
  15. Review
  16. Review
  17. Neuroinflammation and Pediatric Chronic Pain - A Review.Current pain and headache reports · 2026
    Review
  18. Article
  19. Article
  20. Review

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

7 authors at 2 institutions in 2 countries.

Xiao-Xia FangDepartment of Human Anatomy, School of Medicine, Nantong University, Nantong, China.
Meng-Nan ZhaiDepartment of Human Anatomy, School of Medicine, Nantong University, Nantong, China.
Meixuan ZhuDepartment of Psychiatry, Massachusetts General Hospital, Harvard Medical School, Charlestown, MA, USA.
Cheng HeDepartment of Human Anatomy, School of Medicine, Nantong University, Nantong, China.
Heng WangDepartment of Human Anatomy, School of Medicine, Nantong University, Nantong, China.
Juan WangDepartment of Human Anatomy, School of Medicine, Nantong University, Nantong, China.
Zhi-Jun ZhangDepartment of Human Anatomy, School of Medicine, Nantong University, Nantong, China.ORCID 0000-0001-6996-8683
Nantong University · CNHarvard University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Chronic pain is a refractory health disease worldwide causing an enormous economic burden on individuals and society. Accumulating evidence suggests that inflammation in the peripheral nervous system (PNS) and central nervous system (CNS) is the major factor in the pathogenesis of chronic pain. The inflammation in the early- and late phase may have distinctive effects on the initiation and resolution of pain, which can be viewed as friend or foe. On the one hand, painful injuries lead to the activation of glial cells and immune cells in the PNS, releasing pro-inflammatory mediators, which contribute to the sensitization of nociceptors, leading to chronic pain; neuroinflammation in the CNS drives central sensitization and promotes the development of chronic pain. On the other hand, macrophages and glial cells of PNS and CNS promote pain resolution via anti-inflammatory mediators and specialized pro-resolving mediators (SPMs). In this review, we provide an overview of the current understanding of inflammation in the deterioration and resolution of pain. Further, we summarize a number of novel strategies that can be used to prevent and treat chronic pain by controlling inflammation. This comprehensive view of the relationship between inflammation and chronic pain and its specific mechanism will provide novel targets for the treatment of chronic pain.

Indexed as

Chronic PainCentral Nervous SystemCentral Nervous System SensitizationHumansInflammationNeurogliachronic painglial cellInflammationpro-inflammatory mediatorspecialized pro-resolving mediator

Identifiers

PMID37220667
PMCPMC10214073
OpenAlexW4377861199

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.