抄録
Apoptosis occurs in a variety of physiologic situations, including embryogenesis, and plays a crucial role in normal tissue homeostasis, however, a breakdown in the delicate balance between cell survival and apoptosis has been implicated in the pathogenesis of a number of rheumatic diseases. Recent studies have revealed that the signals leading to apoptotic cell death are regulated by the molecular interactions among a set of gene products, thus, it is possible to speculate that the expression of apoptosis-related molecules in situ is modulated by various humoral and/or cellular factors, which may contribute to the characteristic phenotype of each human autoimmune disease. Rheumatoid arthritis (RA) is a joint-affecting disease, which is characterized by the hyperplasia of synovial tissues with periarticular bone destruction (bone loss), thus, the impaired synovial cell apoptosis with the increased susceptibility toward osteoblast apoptosis have been speculated.
We are going to discuss in this review the apoptosis mechanisms involving in the synovial cell hyperplasia, as well as therapeutic implication of apoptosis induction, in patients with RA.
