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
Noise-induced hearing loss (NIHL) is a prevalent cause of sensorineural hearing impairment, in which mitochondrial dysfunction plays a key pathogenic role.
方法
Mitophagy is essential for maintaining mitochondrial quality control.
核心结论
Mitophagy-associated markers and mitochondrial function were assessed by Western blotting, quantitative real-time PCR, mitochondrial DNA (mtDNA) integrity analysis, ATP measurements, and immunohistochemistry/immunofluorescence.；UA treatment significantly reduced auditory threshold shifts compared with the untreated group.；The expression levels of mitophagy-related proteins and genes, including PINK1, Parkin, and BNIP3, were significantly increased in the UA-treated group.；UA attenuates NIHL by enhancing mitophagy-associated markers and preserving mitochondrial function in the cochlea.
局限
（原文未给出可直接抽取的对应表述）
对本项目的价值
高价值：Urolithin A（线粒体自噬激活剂）是已进入人体临床的少数 geroprotector 候选，本文把它扩展到噪声性听力损失并给出耳蜗 mitophagy 标志物读出，支持感觉器官衰老的跨界效应假设。 ｜ 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：Urolithin A Attenuates Noise-induced Hearing Loss and Is Associated With Increased Cochlear Mitophagy Markers.
- 期刊与标识：In vivo (Athens, Greece) · PMID 42957222 · DOI 10.21873/invivo.14481
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。