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Rheumatology Advance Access originally published online on December 16, 2003
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Rheumatology 2004; 43: 405-407
Rheumatology Vol. 43 No. 4 (c) British Society for Rheumatology 2004; all rights reserved

Editorial

Apoptosis a relevant therapeutic target in rheumatoid arthritis?

M. D. Smith and J. G. Walker

Repatriation General Hospital, Rheumatology Unit, Adelaide, South Australia, Australia

Correspondence to: M. D. Smith. malcolm.smith@rgh.sa.gov.au

The first 150 words of the full text of this article appear below.

Rheumatoid arthritis (RA) is a chronic inflammatory disorder with a heterogeneous course. Early histological features include synovial lining hyperplasia, angiogenesis and mononuclear cell infiltrates [1]. Hyperplastic changes encompass both macrophage-like synovial cells and fibroblast-like synovial cells. The fibroblast-like synoviocytes exhibit pre-neoplastic characteristics, with invasive tendencies and expression of proto-oncogenes [2]. In the later stages of disease, synovial proliferation is reduced and often replaced by connective tissue [3]. One explanation for the synovial proliferation is an imbalance between cell proliferation and apoptosis or programmed cell death. For this reason, the induction of apoptosis has been proposed as a potential therapeutic approach (Table 1).


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  		TABLE 1. Potential therapeutic targets to induce apoptosis in rheumatoid arthritis (adapted from [21])

 
Apoptosis is an evolutionarily conserved cell death pathway that occurs in a variety of physiological situations. An apoptotic stimulus induces an initiation and commitment phase, followed . . . [Full Text of this Article]


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