title: Apoptosis of rheumatoid arthritis fibroblast-like synoviocytes: possible roles of nitric oxide and the thioredoxin 1.
abstract: Rheumatoid arthritis is a chronic inflammatory disease characterized by synovial hyperplasia and progressive joint destruction. The impaired apoptosis of rheumatoid arthritis fibroblast-like synoviocytes (RA-FLS) is pivotal in this process. However, the molecular mechanisms responsible for the reduced apoptosis are not fully understood. Both nitric oxide and thioredoxin 1 as two important mediators are widely investigated in the pathogenesis of rheumatoid arthritis. Interestingly, studies have showed that thioredoxin 1 may serve as a master regulator of S-nitrosylation of caspase-3 to fine-tune apoptosis in vivo. Thus, it is anticipated that further investigations on the role of thioredoxin 1 in the S-nitrosylation and denitrosylation of caspase-3 in RA-FLS will likely provide a novel understanding of mechanisms implicated in the impaired apoptosis of RA-FLS. In this paper, we will provide an overview on pathways involved in the reduced apoptosis of RA-FLS and then discuss specially the possible roles of nitric oxide and the thioredoxin 1 redox system associated with apoptosis of RA-FLS.
authors.affiliation: School of Pharmacy, Shanghai Jiao Tong University, Shanghai 200240, China. lihl@sjtu.edu.cn
authors.forename: Huili
authors.initials: H
authors.lastname: Li
authors.forename: Ajun
authors.initials: A
authors.lastname: Wan
mesh_terms: D000818:Animals; D017209:Apoptosis / Q000502:physiology; D001172:Arthritis, Rheumatoid / Q000378:metabolism*; D006801:Humans; D009569:Nitric Oxide / Q000378:metabolism*; D013583:Synovial Membrane / Q000166:cytology* / Q000378:metabolism*; D013879:Thioredoxins / Q000378:metabolism*
chemical_list: D009569:Nitric Oxide; D013879:Thioredoxins