期刊
OSTEOARTHRITIS AND CARTILAGE
卷 29, 期 10, 页码 1389-1398出版社
ELSEVIER SCI LTD
DOI: 10.1016/j.joca.2021.07.003
关键词
Tyrosine kinases; Chondrocyte hypertrophy; Disease modifying OA drugs
资金
- European Union's Horizon 2020 Research and Innovation Programme, Marie Sklodowska-Curie grant [721432]
Osteoarthritis (OA) is a major global health issue characterized by joint pain and inflammation. Tyrosine kinases have been associated with chondrocyte hypertrophy, highlighting their potential as therapeutic targets for OA.
Osteoarthritis (OA) is a major health problem worldwide that affects the joints and causes severe disability. It is characterized by pain and low-grade inflammation. However, the exact pathogenesis remains unknown and the therapeutic options are limited. In OA articular chondrocytes undergo a phenotypic transition becoming hypertrophic, which leads to cartilage damage, aggravating the disease. Therefore, a therapeutic agent inhibiting hypertrophy would be a promising disease-modifying drug. The therapeutic use of tyrosine kinase inhibitors has been mainly focused on oncology, but the Food and Drug Administration (FDA) approval of the Janus kinase inhibitor Tofacitinib in Rheumatoid Arthritis has broadened the applicability of these compounds to other diseases. Interestingly, tyrosine kinases have been associated with chondrocyte hypertrophy. In this review, we discuss the experimental evidence that implicates specific tyrosine kinases in signaling pathways promoting chondrocyte hypertrophy, highlighting their potential as therapeutic targets for OA. (c) 2021 The Authors. Published by Elsevier Ltd on behalf of Osteoarthritis Research Society International. This is an open access article under the CC BY license (http://creativecommons.org/licenses/by/4.0/).
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