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Table 1 FLS in disease initiation, perpetuation, and terminal joint destruction

From: Fibroblast-like synoviocyte metabolism in the pathogenesis of rheumatoid arthritis

FLS activated via FLS response
FLS in arthritis initiation
TLR endogenous ligands
Activated complement
Autoantibodies or immune complexes
Synoviocyte-like macrophage mediators
Mechanical stimulus
Activation markers
Changes in metabolism
Signaling pathway activation
Synovial hyperplasia
Increased expression of adhesion molecules
FLS in arthritis perpetuation
Cytokine receptors
Changes in metabolism
Bioactive metabolites
Signaling pathway activation
Adhesion molecules
Cytokine and chemokine release
Recruitment of B and T cells and macrophages to sublining
Increase of HLA antigen presentation
Proteoglycan damage in cartilage surface
Mitochondrial compensatory response
FLS in joint destruction
Immune cell mediators (cytokines, ligands)
Epigenetic changes, hypomethylation, hyperacetylation
Somatic and mitochondrial mutation
Chronic metabolic changes
Tumor-like transformation
Attachment to cartilage
Migration and invasion
MMP production
RANKL expression
Resistance to apoptosis
  1. MMP metalloprotease, RANKL receptor activator of nuclear factor kappa-B ligand, TLR Toll-like receptor