ReviewInternational journal of general medicine2025
Signal Transduction Pathways Involved in Acupuncture-Mediated Inhibition of Synovitis in Knee Osteoarthritis: A Comprehensive Review.
Review in International journal of general medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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.
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.
Who cites it
3 citing papers in PubMed.
- Acupuncture alleviates postoperative hemorrhoid pain by modulating the P2X7/ERK pathway.Purinergic signalling · 2026Article
- Pain Modulation, Inflammation-Regulatory Mechanisms, and Translational Boundaries of Evidence for Acupuncture-Related Therapies in Knee Osteoarthritis: A Structured Narrative Review.Journal of pain research · 2026Review
- MAPK Pathway Activation Patterns in the Synovium Reveal ERK1/2 and EGFR as Key Players in Osteoarthritis.Biomedicines · 2025Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Knee osteoarthritis (KOA) is a prevalent degenerative joint disorder characterized by synovitis, cartilage degradation, and nociception, in which dysregulated immune responses and excessive pro‑inflammatory mediators drive synovial inflammation as a central pathogenic mechanism. Acupuncture, a cornerstone of traditional Chinese medicine, has demonstrated clinical efficacy in alleviating pain, attenuating synovial pathology, and restoring joint function in KOA. In this review, we systematically elucidate the molecular mechanisms by which acupuncture suppresses synovial inflammation, focusing on its multimodal modulation of five critical signaling cascades: norepinephrine (NE) signaling, the TLRs/NF‑κB pathway, the MCP1/CCR2 axis, the NLRP3 inflammasome, and the Ras‑Raf‑MEK1/2‑ERK1/2 pathway. Relevant studies published between 2000 and 2024 were identified through comprehensive searches of PubMed and CNKI using terms such as "acupuncture + synovitis + MAPK pathway", "acupuncture + inflammation", and "knee osteoarthritis + molecular mechanisms". English and Chinese peer‑reviewed articles reporting preclinical or clinical data on acupuncture's effects in KOA synovitis were included, while studies lacking mechanistic insights or unrelated to synovial inflammation were excluded. Study validity, risk of bias, and methodological rigor were appraised using the GRADE framework. Cumulative evidence indicates that acupuncture exerts anti‑inflammatory and chondroprotective effects by orchestrating multi‑pathway regulation, thereby reducing inflammatory mediators, promoting tissue repair, and improving joint function. As a promising adjunct to pharmacotherapy-particularly in early‑stage KOA-acupuncture merits further validation through large‑scale clinical trials aimed at optimizing treatment parameters, confirming long‑term efficacy, and exploring synergistic combinations with emerging therapies to enable personalized KOA management.
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Registered trials
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.