The Role of CCL3 in the Pathogenesis of Rheumatoid Arthritis.
Ying-Li YangXiao-Feng LiBiao SongSha WuYuan-Yuan WuCheng HuangJun LiPublished in: Rheumatology and therapy (2023)
Rheumatoid arthritis (RA) is a chronic autoimmune disease of unexplained causes. Its pathological features include synovial tissue hyperplasia, inflammatory cell infiltration in joint cavity fluid, cartilage bone destruction, and joint deformation. C-C motif chemokine ligand 3 (CCL3) belongs to inflammatory cell chemokine. It is highly expressed in inflammatory immune cells. Increasingly, studies have shown that CCL3 can promote the migration of inflammatory factors to synovial tissue, the destruction of bone and joint, angiogenesis, and participate in the pathogenesis of RA. These symptoms indicate that the expression of CCL3 is highly correlated with RA disease. Therefore, this paper reviews the possible mechanism of CCL3 in the pathogenesis of RA, which may provide some new insights for the diagnosis and treatment of RA.
Keyphrases
- rheumatoid arthritis
- disease activity
- liver injury
- liver fibrosis
- drug induced
- ankylosing spondylitis
- oxidative stress
- interstitial lung disease
- single cell
- cell therapy
- bone mineral density
- multiple sclerosis
- systemic lupus erythematosus
- systemic sclerosis
- randomized controlled trial
- stem cells
- systematic review
- poor prognosis
- endothelial cells
- postmenopausal women
- physical activity
- sleep quality
- vascular endothelial growth factor
- meta analyses
- bone loss
- binding protein
- idiopathic pulmonary fibrosis