时间标签：数据日期 2026-11-03 · 生成时间 2026-11-03 05:30（Asia/Shanghai）｜ 检索窗口 PubMed edat 2026/10/31 – 2026/11/03 ｜ 情报发生日期 2026-11-03
研究问题
From this perspective, the significance of macrophage plasticity in DMSDs should be understood in terms of whether macrophages can promote termination of tissue stress, resolution of inflammation, and restoration of a repair-permissive microenvironment.；In experimental design, this approach shifts emphasis from marker-defined macrophage states toward identifying the relevant macrophage population in its spatial and disease-stage context, testing its disease-relevant function, and establishing whether that function is causally linked to tissue degeneration or repair.；In therapeutic development, it shifts emphasis from generic macrophage repolarization or pathway inhibition toward selecting disease-relevant macrophage functions and determining whether they can be modified within the anatomical, cellular, and delivery constraints of the affected niche while producing meaningful tissue-level benefit.
方法
（原文未给出可直接抽取的对应表述）
核心结论
These findings indicate that macrophage function is strongly dependent on disease context and tissue niche, and cannot be interpreted apart from specific tissue architecture, disease stage, and repair demand.；Taken together, these functional and cellular data make OA one of the most suitable DMSDs for macrophage-directed immunomodulation, because the joint cavity is relatively accessible, synovial macrophages are closely linked to disease phenotypes, and local delivery is clinically feasible.；Together, these findings suggest that macrophage heterogeneity in IVDD is shaped by both structural access to the disc and subsequent adaptation to distinct local microenvironments.
局限
However, placing these diseases within a shared category does not mean that they arise from the same tissue environment or follow a unified pathogenic mechanism.；Thus, although DMSDs share clinical and pathological contexts, they cannot be reduced to a single mechanism-driven disease spectrum.
对本项目的价值
中等价值：属「营养感知—自噬—蛋白稳态轴」方向；干细胞 / 再生 / 重编程栏目可用作本项目文献库与综述素材。 ｜ 价值分 2.6/5（★★★☆☆）
全文来源
PubMed PMC JATS（正文 90,252 字符，题名指纹 1.00，已过 DOI 逐字 + 题名指纹 + 正文长度三重归属校验）
原文题录
- 中文题名：退行性肌肉骨骼疾病中的巨噬细胞重编程：从组织微生态到治疗转化
- 英文标题：Macrophage reprogramming in degenerative musculoskeletal diseases: From tissue-niche biology to therapeutic translation.
- 期刊与标识：J Orthop Translat · PMID 42964394 · DOI 10.1016/j.jot.2026.101244 · PMC PMC13720371 · EDAT 2026-10-31