Evidence map›Paper›PMID 40629417›Full record

ArticleJournal of orthopaedic surgery and research2025

Acupressure attenuates fibromyalgia central sensitization via MAPK phosphorylation-mediated neuroinflammation regulation.

Kezhi Liu, Yuye Lin, Tianyu Rao, Yuting Huang, Yu Kan, Jun Liao

Abstract read
In one paragraph

Article in Journal of orthopaedic surgery and research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
–field-weighted citation impact
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

8 citing papers in PubMed.

  1. Article
  2. Article
  3. Review
  4. Review
  5. Article
  6. Article
  7. Review
  8. CRISPR-guided nanotherapy for rare central sensitization syndromes.Annals of medicine and surgery (2012) · 2025
    Article
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

6 authors.

Kezhi Liu *College of acupuncture and moxibustion and Massage, Fujian University of Traditional Chinese Medicine, Fuzhou, 350122, Fujian Province, China.
Yuye Lin *College of acupuncture and moxibustion and Massage, Fujian University of Traditional Chinese Medicine, Fuzhou, 350122, Fujian Province, China.
Tianyu RaoCollege of acupuncture and moxibustion and Massage, Fujian University of Traditional Chinese Medicine, Fuzhou, 350122, Fujian Province, China.
Yuting HuangCollege of acupuncture and moxibustion and Massage, Fujian University of Traditional Chinese Medicine, Fuzhou, 350122, Fujian Province, China. 836529518@qq.com.
Yu KanCollege of acupuncture and moxibustion and Massage, Fujian University of Traditional Chinese Medicine, Fuzhou, 350122, Fujian Province, China. 2019035@fjtcm.edu.cn.
Jun LiaoCollege of acupuncture and moxibustion and Massage, Fujian University of Traditional Chinese Medicine, Fuzhou, 350122, Fujian Province, China. 2007065@fjtcm.edu.cn.

Funding

the National Natural Science Foundation of China 82074181the National Natural Science Foundation of China 82204908the National Natural Science Foundation of China 82374202
6 · The paper itself

Abstract

backgroundFibromyalgia syndrome (FMS) is a chronic musculoskeletal disorder with unclear pathogenesis and a lack of targeted therapies. Central sensitization has emerged as a key mechanism that drives its pathophysiology. Although clinical studies support the efficacy of acupressure (ACP) in alleviating FMS symptoms, its underlying mechanisms remain poorly understood. This study investigates how ACP modulates central sensitization and inflammatory pathways in a rat model of FM.

methodsAn FM rat model was developed to evaluate the efficacy of ACP therapy. Pain sensitivity and emotional distress were assessed using behavioral tests. Molecular analyses, including Western blot and immunofluorescence, were used to measure MAPK pathway activity (phosphorylation of p38 MAPK and JNK MAPK), glial cell activation (microglia and astrocytes), and inflammatory cytokine levels (TNF-ɑ, IL-6). Post-translational modifications were analyzed to explore anti-inflammatory mechanisms.

resultsACP therapy significantly reduced pain sensitivity in FM rats. Mechanistically, ACP inhibited phosphorylation of p38 MAPK and JNK MAPK, suppressed glial cell activation, reduced pro-inflammatory cytokine release, and eventually attenuated central sensitization. The anti-inflammatory effects were mediated primarily by regulating post-translational modifications rather than altering protein synthesis or degradation. Additionally, ACP restored muscle function and demonstrated therapeutic effects on somatic manifestations of FMS.

conclusionACP exerts multimodal therapeutic effects on FMS through dual modulation of MAPK signaling, which targets central sensitization and inflammation through precision-driven post-translational regulation. Its ability to alleviate physical symptoms highlights its potential as a targeted intervention for FMS. These findings provide mechanistic insights into ACP's clinical efficacy and support its integration into FMS management strategies.

Indexed as

AcupressureCentral Nervous System SensitizationFibromyalgiaMAP Kinase Signaling SystemNeuroinflammatory DiseasesAnimalsDisease Models, AnimalMalep38 Mitogen-Activated Protein KinasesPhosphorylationRatsRats, Sprague-Dawleyp38 Mitogen-Activated Protein KinasesAcupressureFibromyalgia syndromeMAPKPhosphorylated

Identifiers

PMID40629417
PMCPMC12235862

What Socratic holds

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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 Socratic graph.