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.

骨关节炎 (OA) 是世界范围内的主要健康问题，会影响关节并导致严重残疾。它的特点是疼痛和低度炎症。然而，确切的发病机制仍然未知，治疗选择有限。在 OA 关节软骨细胞经历表型转变变成肥大，这导致软骨损伤，加重疾病。因此，抑制肥大的治疗剂将是一种有前途的疾病改善药物。酪氨酸激酶抑制剂的治疗用途主要集中在肿瘤学上，但食品和药物管理局 (FDA) 批准 Janus 激酶抑制剂 Tofacitinib 治疗类风湿性关节炎扩大了这些化合物对其他疾病的适用性。有趣的是，酪氨酸激酶与软骨细胞肥大有关。