Level D· Scientific groundwork from lab and animal studiesNarrative ReviewEurope PMCOpen access

Pyroptosis for osteoarthritis treatment: insights into cellular and molecular interactions inflammatory

Lin M., Zhang C., Li H., Li K., Gou S., He X.

Narrative Review on Osteoarthritis, Cartilage Damage, Chronic Inflammation, published in Front Immunol (2025) — summary generated from the PubMed abstract.

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Level D· Scientific groundwork from lab and animal studiesEvidence level of this study

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

  • Level A · Stronger Clinical Evidence
  • Level B · Emerging clinical evidence with positive signals
  • Level C · Early human research exploring benefits
  • Level D · Scientific groundwork from lab and animal studies
  • Emerging · Emerging topic under active research
Read the A–D evidence level guide

This page is generated from the PubMed record. The Thai description is an automated summary of bibliographic fields and the abstract, not a full translation, and is not medical advice.

Study type
Narrative Review
Journal
Front Immunol (2025)
Reported sample size
—
Source database
Europe PMC
PMID
40236711
PMCID
PMC11996656
DOI
10.3389/fimmu.2025.1556990
Citations
11

Abstract (original English)

Osteoarthritis (OA) is a widely prevalent chronic degenerative disease often associated with significant pain and disability. It is characterized by the deterioration of cartilage and the extracellular matrix (ECM), synovial inflammation, and subchondral bone remodeling. Recent studies have highlighted pyroptosis-a form of programmed cell death triggered by the inflammasome-as a key factor in sustaining chronic inflammation. Central to this process are the inflammatory cytokines interleukin-1β (IL-1β) and interleukin-18 (IL-18), which play crucial roles mediating intra-articular pyroptosis through the NOD-like receptor protein 3 (NLRP3) inflammasome. This paper investigates the role of the pyroptosis pathway in perpetuating chronic inflammatory diseases and its linkage with OA. Furthermore, it explores the mechanisms of pyroptosis, mediated by nuclear factor κB (NF-κB), the purinergic receptor P2X ligand-gated ion channel 7 (P2X7R), adenosine monophosphate (AMP)-activated protein kinase (AMPK), and hypoxia-inducible factor-1α (HIF-1α). Additionally, it examines the interactions among various cellular components in the context of OA. These insights indicate that targeting the regulation of pyroptosis presents a promising therapeutic approach for the prevention and treatment of OA, offering valuable theoretical perspectives for its effective management.

What this study does not prove

  • • This study does not prove SVF is an approved treatment or a replacement for standard care.
  • • This is a narrative review: it collects no new patient data and does not systematically appraise evidence quality.

Evidence level

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

How we grade evidence
AnimalsHumansOsteoarthritisInflammationNF-kappa BSignal TransductionHypoxia-Inducible Factor 1, alpha SubunitInterleukin-1betaReceptors, Purinergic P2X7Inflammasomes

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