Tyrosine kinases regulate chondrocyte hypertrophy: promising drug targets for Osteoarthritis

M. N. Ferrao Blanco, H. Domenech Garcia, L. Legeai-Mallet, G. J.V.M. van Osch*

*Corresponding author for this work

Research output: Contribution to journalReview articlepeer-review

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Abstract

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.

Original languageEnglish
Pages (from-to)1389-1398
JournalOsteoarthritis and Cartilage
Volume29
Issue number10
DOIs
Publication statusPublished - 2021

Keywords

  • Chondrocyte hypertrophy
  • Disease modifying OA drugs
  • Tyrosine kinases

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