时间标签：数据日期 2026-11-01 · 生成时间 2026-11-01 05:30（Asia/Shanghai）｜ 检索窗口 PubMed edat 2026/10/31–2026/11/01 ｜ 情报发生日期 2026-11-01
证据级别：摘要级。本条依据 PubMed 结构化摘要与元数据撰写，付费墙全文未获取、未逐节核验，本站未做任何数值推算补全。
研究问题
The study aimed to investigate the mechanism by which DEAD-box helicase 6 (DDX6) regulates ferroptosis by interacting with cytoplasmic polyadenylation element-binding protein 1 (CPEB1) and contributes to OA progression by regulating…
方法
In vivo, we used 10-week-old mice with osteoblast-specific conditional knockout of Ddx6 (Ddx6fl/fl OC-Cre+) and intra-articular injection of ferrostatin-1 in a destabilization of the medial meniscus-induced OA model to evaluate effects on…
核心结论
Expression levels of proteins associated with ferroptosis, osteosclerosis, and H-type microangiogenesis were measured following DDX6 and CPEB1 overexpression or knockdown using lentiviral and small-interfering RNA transfection.；Conditional knockout of Ddx6 reduced subchondral microvascular infiltration and alleviated cartilage destruction, whereas intra-articular ferrostatin-1 injection showed even greater protective effects.
局限
（原文未给出可直接抽取的对应表述）
对本项目的价值
临床前机制证据，需评估物种外推与剂量可行性：线粒体是衰老干预的共同下游效应器，可用于跨器官效应的统一读数。 ｜ 价值分 1.2/5（★☆☆☆☆）
全文来源
未取到全文 → 本卡为摘要级解读，未核验全文
原文题录
- 英文标题：Targeting DDX6 attenuates osteoarthritis progression by inhibiting CPEB1-mediated ferroptosis in subchondral bone.
- 期刊与标识：Chinese medical journal · PMID 42951868 · DOI 10.1097/cm9.0000000000004335
B 级证据分级：B 级（同行评议临床前研究，主要为动物模型）
本文核心结论来自动物模型或体外细胞学，属临床前证据，不能外推至人体。「延长健康寿命」「改善功能」等表述在小鼠中的意义，与人类临床结局之间仍有距离。
关于本文的文献来源：本站依据 IMA 知识库「五刊监控·深度文献卡片」（SOP §4.2 摘要级）撰写，依据期刊公开摘要与 PubMed 元数据；付费墙全文未获取之处已标注「待补全文」，未做任何数值推算补全。