Zou Xiongfei, Xu Hongjun, Qian Wenwei
Department of Orthopedic Surgery, Peking Union Medical College Hospital, Beijing, China.
Orthop Surg. 2025 Jan;17(1):22-35. doi: 10.1111/os.14302. Epub 2024 Dec 5.
Osteoarthritis (OA) is a prevalent degenerative disorder that severely impacts quality of life due to pain and disability. Although the pathophysiology of OA remains incompletely understood, recent research highlights the role of synovial inflammation in OA onset and progression, driven primarily by inflammatory infiltrates, especially macrophages, in the synovium. These macrophages respond to the local microenvironment, polarizing into either pro-inflammatory (M1) or anti-inflammatory (M2) subtypes. This review focuses on the role of macrophage polarization in OA pathogenesis and treatment, emphasizing how M1/M2 polarization is influenced by pathways such as STAT, NF-κB, caspase, and MAPK. These pathways induce low-grade inflammation within OA-affected joints, altering chondrocyte metabolism, inhibiting cartilage repair, and impairing mesenchymal stem cell chondrogenesis, thereby contributing to OA progression. Additionally, this review discusses potential therapies targeting macrophage polarization, encompassing compounds, proteins, cells, and microRNAs, to offer insights into novel treatment strategies for OA.
骨关节炎（OA）是一种常见的退行性疾病，由于疼痛和残疾严重影响生活质量。尽管OA的病理生理学仍未完全了解，但最近的研究强调了滑膜炎症在OA发病和进展中的作用，这主要是由滑膜中的炎症浸润，特别是巨噬细胞驱动的。这些巨噬细胞对局部微环境作出反应，极化为促炎（M1）或抗炎（M2）亚型。本综述重点关注巨噬细胞极化在OA发病机制和治疗中的作用，强调M1/M2极化如何受到STAT、NF-κB、半胱天冬酶和MAPK等途径的影响。这些途径在OA受累关节内引发低度炎症，改变软骨细胞代谢，抑制软骨修复，并损害间充质干细胞软骨生成，从而促进OA进展。此外，本综述讨论了针对巨噬细胞极化的潜在疗法，包括化合物、蛋白质、细胞和微小RNA，以提供对OA新治疗策略的见解。
