Evidence map›Paper›PMID 35501933›Full record

ReviewInflammation and regeneration2022

Neuroplasticity related to chronic pain and its modulation by microglia.

Shin-Ichiro Hiraga, Takahide Itokazu, Mariko Nishibe, Toshihide Yamashita

Open access · goldAbstract readReview
In one paragraph

Review in Inflammation and regeneration, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
49citing papers in PubMed, 1 pooled it
8.8field-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

49 citing papers in PubMed, 1 synthesis or guideline pooled it, 82 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Review
  4. Review
  5. Review
  6. Article
  7. Article
  8. Kinesiophobia and Work Disability in Fibromyalgia: Cognitive Mediation in a Population-Based Study of Women.European journal of investigation in health, psychology and education · 2026
    Article
  9. Review
  10. Caudal Granular Insular Cortex to Somatosensory Cortex I: A Critical Pathway for the Transition of Acute to Chronic Pain.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2026
    Article
  11. Article
  12. Article
  13. Review
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  17. Review
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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

4 authors at 1 institution in 1 country.

Shin-Ichiro HiragaDepartment of Neuro-Medical Science, Graduate School of Medicine, Osaka University, Suita, Osaka, Japan.
Takahide ItokazuDepartment of Neuro-Medical Science, Graduate School of Medicine, Osaka University, Suita, Osaka, Japan. t.itokazu@molneu.med.osaka-u.ac.jp.
Mariko NishibeCenter for Strategic Innovative Dentistry, Graduate School of Dentistry, Osaka University, Suita, Osaka, Japan.
Toshihide YamashitaDepartment of Neuro-Medical Science, Graduate School of Medicine, Osaka University, Suita, Osaka, Japan. yamashita@molneu.med.osaka-u.ac.jp.
Osaka University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Neuropathic pain is often chronic and can persist after overt tissue damage heals, suggesting that its underlying mechanism involves the alteration of neuronal function. Such an alteration can be a direct consequence of nerve damage or a result of neuroplasticity secondary to the damage to tissues or to neurons. Recent studies have shown that neuroplasticity is linked to causing neuropathic pain in response to nerve damage, which may occur adjacent to or remotely from the site of injury. Furthermore, studies have revealed that neuroplasticity relevant to chronic pain is modulated by microglia, resident immune cells of the central nervous system (CNS). Microglia may directly contribute to synaptic remodeling and altering pain circuits, or indirectly contribute to neuroplasticity through property changes, including the secretion of growth factors. We herein highlight the mechanisms underlying neuroplasticity that occur in the somatosensory circuit of the spinal dorsal horn, thalamus, and cortex associated with chronic pain following injury to the peripheral nervous system (PNS) or CNS. We also discuss the dynamic functions of microglia in shaping neuroplasticity related to chronic pain. We suggest further understanding of post-injury ectopic plasticity in the somatosensory circuits may shed light on the differential mechanisms underlying nociceptive, neuropathic, and nociplastic-type pain. While one of the prominent roles played by microglia appears to be the modulation of post-injury neuroplasticity. Therefore, future molecular- or genetics-based studies that address microglia-mediated post-injury neuroplasticity may contribute to the development of novel therapies for chronic pain.

Indexed as

CNS injuryMicrogliaNeuroplasticityNociplastic painPNS injuryThalamic hemorrhage

Identifiers

PMID35501933
PMCPMC9063368
OpenAlexW4225310650

What OpenQuestion holds

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LicenceCC BY
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.