TY - JOUR
T1 - Apoptosis in rheumatoid arthritis
T2 - Friend or foe
AU - Liu, Hongtao
AU - Pope, Richard M.
N1 - Funding Information:
This work was supported by the National Institutes of Health (Grants AR048269 and AR049217).
PY - 2004/8
Y1 - 2004/8
N2 - A better understanding of the mechanisms that contribute to the resistance of synovial macrophages and fibroblasts to apoptosis will not only provide better insights into the mechanisms contributing to the perpetuation of rheumatoid arthritis (RA) but will also help identify targets for the development of novel, more effective, and long-lasting therapies for the treatment of patients with RA. To avoid toxicity, such as the induction of apoptosis of critical organs, the mechanisms by which these molecules are targeted and therapy delivered must be carefully selected, using the insights obtained from studies characterizing the mechanisms that promote chronic inflammation.
AB - A better understanding of the mechanisms that contribute to the resistance of synovial macrophages and fibroblasts to apoptosis will not only provide better insights into the mechanisms contributing to the perpetuation of rheumatoid arthritis (RA) but will also help identify targets for the development of novel, more effective, and long-lasting therapies for the treatment of patients with RA. To avoid toxicity, such as the induction of apoptosis of critical organs, the mechanisms by which these molecules are targeted and therapy delivered must be carefully selected, using the insights obtained from studies characterizing the mechanisms that promote chronic inflammation.
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U2 - 10.1016/j.rdc.2004.04.010
DO - 10.1016/j.rdc.2004.04.010
M3 - Review article
C2 - 15261344
AN - SCOPUS:3142776251
VL - 30
SP - 603
EP - 625
JO - Rheumatic Disease Clinics of North America
JF - Rheumatic Disease Clinics of North America
SN - 0889-857X
IS - 3
ER -