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
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摘要（PubMed 原文节选）
Bone marrow macrophages (BMMs) coordinate skeletal remodelling, haematopoietic niche function, immune surveillance, and tissue repair. Whether a persistent senescent state in BMMs is a causal driver of skeletal ageing, however, remains unresolved. The central challenge is both definitional and causal: macrophages may be quiescent, terminally differentiated, chronically activated, tolerant, or metabolically dysfunctional, whereas commonly used senescence markers-including p16INK4a, p21CIP1, senescence-associated β-galactosidase activity, and individual senescence-associated secretory phenotype factors-lack diagnostic specificity when used in isolation. In this critical Review, we distinguish …
对本项目的价值
中等价值：属「衰老细胞清除 / SASP 轴」方向；细胞衰老 / senolytics / SASP栏目可用作本项目文献库与综述素材。 ｜ 价值分 2.2/5（★★☆☆☆）
全文不可及原因
无 PMCID 且 OpenAlex / Unpaywall 未提供可下载 OA PDF
原文题录
- 中文题名：衰老巨噬细胞作为骨骼衰老的中枢枢纽：机制、微生态破坏与系统性后果
- 英文标题：The Senescent Macrophage as a Central Hub in Skeletal Aging: Mechanisms, Niche Disruption, and Systemic Consequences.
- 期刊与标识：Ageing Res Rev · PMID 42966513 · DOI 10.1016/j.arr.2026.103431 · EDAT 2026-10-31