Cell-specific epigenetic drivers of pathogenesis in rheumatoid arthritis.
Nisha NairAnne BartonAnthony G WilsonPublished in: Epigenomics (2021)
Rheumatoid arthritis is a complex, inflammatory autoimmune disease, which is characterized by pain, swelling and joint damage driven by the altered behavior of a number of different cell types such as synovial fibroblasts macrophages and lymphocytes. The mechanism underlying pathogenesis is unclear but increasing evidence points to altered epigenetic regulation within these cell types which promotes the activated destructive behavior that underlies disease pathogenesis. This review summarizes the key epigenetic modifications in the most important cells types in rheumatoid arthritis, which are associated with disease activity. We also discuss emerging avenues of research focusing on readers of epigenetic markers which may serve to be potential therapeutic targets.
Keyphrases
- rheumatoid arthritis
- disease activity
- systemic lupus erythematosus
- single cell
- ankylosing spondylitis
- dna methylation
- rheumatoid arthritis patients
- cell therapy
- gene expression
- interstitial lung disease
- multiple sclerosis
- induced apoptosis
- oxidative stress
- juvenile idiopathic arthritis
- cell proliferation
- risk assessment
- peripheral blood
- stem cells
- spinal cord
- spinal cord injury
- cell death
- extracellular matrix
- systemic sclerosis