Single-cell profiling identifies hair cell SLC35F1 deficiency as a signature of primate cochlear aging.

IF 17 Q1 CELL BIOLOGY
Guoqiang Sun, Xiaolong Fu, Yandong Zheng, Guodong Hong, Ziyi Liu, Bilan Luo, Jinghui Lei, Dongliang Lv, Miao Chang, Yu Xiao, Siwei Guo, Shuai Ma, Ling Lu, Weiqi Zhang, Juan Carlos Izpisua Belmonte, Jing Qu, Si Wang, Renjie Chai, Guang-Hui Liu
{"title":"Single-cell profiling identifies hair cell SLC35F1 deficiency as a signature of primate cochlear aging.","authors":"Guoqiang Sun, Xiaolong Fu, Yandong Zheng, Guodong Hong, Ziyi Liu, Bilan Luo, Jinghui Lei, Dongliang Lv, Miao Chang, Yu Xiao, Siwei Guo, Shuai Ma, Ling Lu, Weiqi Zhang, Juan Carlos Izpisua Belmonte, Jing Qu, Si Wang, Renjie Chai, Guang-Hui Liu","doi":"10.1038/s43587-025-00896-0","DOIUrl":null,"url":null,"abstract":"<p><p>Cochlear aging causes substantial hearing impairment in older adults, yet primate-specific mechanisms remain poorly characterized. Our comprehensive analysis combining single-cell and histopathological profiling in aging Macaca fascicularis demonstrates progressive cochlear degeneration featuring accelerated sensory hair cell loss, senescent spiral ganglion neurons with elevated neuroinflammation, and marked stria vascularis atrophy. We discovered that downregulation of transmembrane transport proteins, particularly SLC35F1, serves as a critical biomarker of hair cell aging. Functional validation through Slc35f1 knockdown in adult mice successfully recapitulated key aspects of age-related hearing loss, including hair cell degeneration and auditory function decline. Notably, we showed that long-term metformin administration at clinically relevant doses effectively delays cochlear aging in primates. These findings provide fundamental insights into the cellular and molecular basis of primate cochlear aging while establishing a foundation for developing targeted interventions against age-related hearing loss.</p>","PeriodicalId":94150,"journal":{"name":"Nature aging","volume":" ","pages":""},"PeriodicalIF":17.0000,"publicationDate":"2025-06-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Nature aging","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.1038/s43587-025-00896-0","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q1","JCRName":"CELL BIOLOGY","Score":null,"Total":0}
引用次数: 0

Abstract

Cochlear aging causes substantial hearing impairment in older adults, yet primate-specific mechanisms remain poorly characterized. Our comprehensive analysis combining single-cell and histopathological profiling in aging Macaca fascicularis demonstrates progressive cochlear degeneration featuring accelerated sensory hair cell loss, senescent spiral ganglion neurons with elevated neuroinflammation, and marked stria vascularis atrophy. We discovered that downregulation of transmembrane transport proteins, particularly SLC35F1, serves as a critical biomarker of hair cell aging. Functional validation through Slc35f1 knockdown in adult mice successfully recapitulated key aspects of age-related hearing loss, including hair cell degeneration and auditory function decline. Notably, we showed that long-term metformin administration at clinically relevant doses effectively delays cochlear aging in primates. These findings provide fundamental insights into the cellular and molecular basis of primate cochlear aging while establishing a foundation for developing targeted interventions against age-related hearing loss.

单细胞分析鉴定毛细胞SLC35F1缺陷是灵长类耳蜗老化的标志。
耳蜗老化导致老年人严重的听力损伤,但灵长类动物特异性机制仍不清楚。我们的综合分析结合了衰老的猕猴束状体的单细胞和组织病理学分析,显示了进行性耳蜗变性,表现为感觉毛细胞的加速损失,衰老的螺旋神经节神经元,神经炎症升高,以及明显的血管纹萎缩。我们发现跨膜转运蛋白的下调,特别是SLC35F1,是毛细胞衰老的关键生物标志物。通过Slc35f1基因敲除在成年小鼠中的功能验证,成功再现了与年龄相关的听力损失的关键方面,包括毛细胞变性和听觉功能下降。值得注意的是,我们发现长期服用临床相关剂量的二甲双胍可以有效延缓灵长类动物耳蜗老化。这些发现为灵长类动物耳蜗老化的细胞和分子基础提供了基本的见解,同时为开发针对年龄相关性听力损失的针对性干预措施奠定了基础。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
求助全文
约1分钟内获得全文 求助全文
来源期刊
CiteScore
14.70
自引率
0.00%
发文量
0
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
确定
请完成安全验证×
copy
已复制链接
快去分享给好友吧!
我知道了
右上角分享
点击右上角分享
0
联系我们:info@booksci.cn Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。 Copyright © 2023 布克学术 All rights reserved.
京ICP备2023020795号-1
ghs 京公网安备 11010802042870号
Book学术文献互助
Book学术文献互助群
群 号:604180095
Book学术官方微信