Please use this identifier to cite or link to this item: http://hdl.handle.net/2440/117052
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Type: Journal article
Title: Intracellular apoptotic pathways: a potential target for reducing joint damage in rheumatoid arthritis
Author: Williams, B.
Dharmapatni, A.
Crotti, T.
Citation: Inflammation Research, 2018; 67(3):219-231
Publisher: Springer
Issue Date: 2018
ISSN: 1023-3830
1420-908X
Statement of
Responsibility: 
Bonnie Williams, Anak Dharmapatni, Tania Crotti
Abstract: Rheumatoid arthritis (RA) is a chronic autoimmune inflammatory disease that results in both local and systemic bone erosion, causing significant joint deformities and functional disability. The increased number of synovial fibroblasts, inflammatory cells and osteoclasts in RA is associated with reduced apoptosis in these cells. The ability to modulate the cell proliferation or death (particularly apoptosis) is recognised for its immense therapeutic potential. Identifying new therapeutics to assist in stimulating apoptosis within the synovial joints therefore may be beneficial in reducing inflammation and bone loss in RA patients. In this review, the roles of anti-apoptotic proteins that are upregulated in RA synovial joints will be discussed in relation to their actions on bone destruction and inflammation. Evidence recently published suggests that intracellular apoptotic inhibitory molecules can be targeted by current or new therapeutics to reduce joint damage in RA. However, the therapeutics that target these molecules are yet to reach clinical trial stages. Even so it is evident that understanding the upregulation of anti-apoptotic molecules in RA is required to improve treatments currently available for RA patients.
Keywords: Anti-apoptotic proteins; Apoptosis; Bone erosion; Disease-modifying anti-rheumatic drugs; Rheumatoid arthritis; Therapeutics
Rights: © Springer International Publishing AG, part of Springer Nature 2017
RMID: 0030078255
DOI: 10.1007/s00011-017-1116-5
Appears in Collections:Animal and Veterinary Sciences publications

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