Although rheumatoid arthritis affects 1% of the global population, the role of rheumatoid cachexia, which occurs in up to a third of patients, is relatively neglected as research focus, despite its significant contribution to decreased quality of life in patients. A better understanding of the cellular and molecular processes involved in rheumatoid cachexia, as well as its potential treatment, is dependent on elucidation of the intricate interactions of the cells involved, such as myoblasts, fibroblasts and macrophages. Persistent RA-associated inflammation results in a relative depletion of the capacity for regeneration and repair in the satellite cell niche. The repair that does proceed is suboptimal due to dysregulated communication from the other cellular role players in this multi-cellular environment. This includes the incomplete switch in macrophage phenotype resulting in a lingering pro-inflammatory state within the tissues, as well as fibroblast-associated dysregulation of the dynamic control of the extracellular matrix. Additional to this endogenous dysregulation, some treatment strategies for RA may exacerbate muscle wasting and no multi-cell investigation has been done in this context. This review summarizes the most recent literature characterising clinical RA cachexia and links these features to the roles of and complex communication between multiple cellular contributors in the muscle niche, highlighting the importance of a targeted approach to therapeutic intervention.

中文翻译：

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类风湿性恶病质：成肌细胞、巨噬细胞和成纤维细胞在骨骼肌生态位中相互作用的作用未被充分认识

尽管类风湿性关节炎影响全球人口的 1%，但类风湿性恶病质（发生在多达三分之一的患者中）的作用作为研究重点相对被忽视，尽管它对患者生活质量的下降有显着影响。对类风湿性恶病质涉及的细胞和分子过程及其潜在治疗的更好理解取决于对所涉及细胞（例如成肌细胞、成纤维细胞和巨噬细胞）复杂相互作用的阐明。持续的 RA 相关炎症导致卫星细胞生态位再生和修复能力的相对损耗。由于多细胞环境中其他细胞角色的通讯失调，所进行的修复并不理想。这包括巨噬细胞表型的不完全转换，导致组织内挥之不去的促炎状态，以及成纤维细胞相关的细胞外基质动态控制失调。除了这种内源性失调之外，一些 RA 的治疗策略可能会加剧肌肉萎缩，并且在这方面尚未进行多细胞研究。这篇综述总结了表征临床 RA 恶病质的最新文献，并将这些特征与肌肉生态位中多个细胞贡献者的作用和复杂的沟通联系起来，强调了有针对性的治疗干预方法的重要性。