The Ph.D. Program of Biotechnology and Biomedical Industry, China Medical University, Taichung, Taiwan.
Department of Pharmacology, School of Medicine, China Medical University, Taichung, Taiwan; Graduate Institute of Biomedical Sciences, China Medical University, Taichung, Taiwan; Chinese Medicine Research Center, China Medical University, Taichung, Taiwan; Department of Medical Laboratory Science and Biotechnology, College of Medical and Health Science, Asia University, Taichung, Taiwan; Department of Medical Research, China Medical University Hsinchu Hospital, Hsinchu, Taiwan.
Int Immunopharmacol. 2024 Dec 5;142(Pt A):113056. doi: 10.1016/j.intimp.2024.113056. Epub 2024 Aug 31.
Rheumatoid arthritis (RA) and osteoarthritis (OA) are common and debilitating joint disorders affecting millions of individuals worldwide. Despite their distinct pathological features, both conditions share a crucial role of macrophages in disease progression. Macrophages exhibit remarkable plasticity, polarizing into pro-inflammatory M1 or anti-inflammatory M2 phenotypes in response to environmental cues. An imbalance in macrophage polarization, particularly a shift towards the M1 phenotype, contributes to chronic inflammation and joint damage in RA and OA. This review explores the complex interplay between macrophages and various cell types, including T cells, B cells, synovial fibroblasts, osteoclasts, chondrocytes, and adipocytes, in the pathogenesis of these diseases. We discuss the current understanding of macrophage polarization in RA and OA, highlighting the molecular mechanisms involved. Furthermore, we provide an overview of potential therapeutic strategies targeting macrophage polarization, such as disease-modifying anti-rheumatic drugs, traditional Chinese medicine, nanomedicines, proteins, chemical compounds, and physical therapies. By elucidating the precise mechanisms governing macrophage polarization and its interactions with other cells in the joint microenvironment, researchers can identify novel therapeutic targets and develop targeted interventions to alleviate disease progression and improve patient outcomes in RA and OA.
类风湿关节炎（RA）和骨关节炎（OA）是常见的、使人衰弱的关节疾病，影响着全球数以百万计的人群。尽管这两种疾病具有明显不同的病理特征，但它们在疾病进展中都有一个关键的角色，那就是巨噬细胞。巨噬细胞表现出显著的可塑性，能够根据环境线索极化成为促炎的 M1 表型或抗炎的 M2 表型。巨噬细胞极化的失衡，特别是向 M1 表型的转变，导致了 RA 和 OA 中的慢性炎症和关节损伤。这篇综述探讨了巨噬细胞与 T 细胞、B 细胞、滑膜成纤维细胞、破骨细胞、软骨细胞和脂肪细胞等多种细胞类型之间的复杂相互作用，在这些疾病的发病机制中的作用。我们讨论了目前对 RA 和 OA 中巨噬细胞极化的理解，强调了涉及的分子机制。此外，我们还概述了针对巨噬细胞极化的潜在治疗策略，如改善病情的抗风湿药物、中药、纳米药物、蛋白质、化学化合物和物理疗法。通过阐明控制巨噬细胞极化及其与关节微环境中其他细胞相互作用的精确机制，研究人员可以确定新的治疗靶点，并开发靶向干预措施，以减轻 RA 和 OA 的疾病进展并改善患者的预后。
