Senescent synovial fibroblasts accumulate prematurely in rheumatoid arthritis tissues and display an enhanced inflammatory phenotype.
Manuel J Del ReyÁlvaro ValínAlicia UsateguiSandra ErguetaEduardo MartínCristina MunicioJuan D CañeteFrancisco J BlancoGabriel CriadoJosé Luís PablosPublished in: Immunity & ageing : I & A (2019)
Accumulation of senescent cells in ST increases in normal aging and prematurely in RA patients. Senescence of cultured SF is accelerated upon exposure to TNFα or oxidative stress and may contribute to the pathogenesis of synovitis by increasing the production of pro-inflammatory mediators.
Keyphrases
- rheumatoid arthritis
- oxidative stress
- induced apoptosis
- end stage renal disease
- endothelial cells
- dna damage
- disease activity
- newly diagnosed
- ejection fraction
- chronic kidney disease
- gene expression
- peritoneal dialysis
- ankylosing spondylitis
- prognostic factors
- interstitial lung disease
- cell death
- idiopathic pulmonary fibrosis