时间标签：数据日期 2026-10-31 · 生成时间 2026-11-01 05:30（Asia/Shanghai）｜ 检索窗口 PubMed edat 2026/10/28–2026/10/31 ｜ 情报发生日期 2026-10-31
研究问题
However, mammalian SGNs lack regenerative capacity, and their degeneration leads to permanent hearing impairment [].；However, emerging evidence has revealed its widespread expression in neurons [], fibroblasts [], and smooth muscle cells [], indicating its diverse pathophysiological roles.；However, whether CXCR2 is expressed in cochlear SGNs and whether it contributes to auditory signal regulation currently remains unclear.
方法
C57BL/6 mice were obtained from Charles River Laboratories.；The experimental mice were grouped by a simple random sampling method, and the relative assays were performed blindly.；The specimens were permeabilized in 0.1% Triton X-100 and incubated in 10% serum for 60 min at room temperature followed by incubation with primary antibodies: mouse anti-Tuj1 (#801202, Biolegend, CA, USA,), rabbit anti-CXCR2 (#20634-1-AP, Proteintech, USA), rabbit anti-Kv1.1 (#APC-009, Alomone labs, Israel), mouse anti-CtBP2 (#612044, BD Biosciences), mouse anti-GluR2 (#MAB397, Millipore), rabbit anti-Kv1.2 (#APC-010, Alomone labs, Israel), rabbit anti-MBP (#, Abcam, USA) and rabbit anti-Myo7a (#PT-25-6790, Proteus, Ramona, CA, USA), overnight at 4 °C.；Cochlear total RNA was extracted from 2-month-old (2M) mice (5 mice per sample) using TRIzol reagent (Invitrogen, Carlsbad, CA, USA).
核心结论
Our results revealed strong CXCR2 expression in cochlear SGNs, HCs, and the stria vascularis (Fig. ).；Compared with WT mice, both heterozygous (CXCR2+/-) and homozygous CXCR2 knockout (CXCR2-/-) mice at 2 months of age exhibited a significant increase in the ABR threshold, indicating hearing impairment (Fig. ).；Compared with age-matched WT mice, CXCR2+/- mice displayed elevated ABR thresholds at 1 month of age, which further increased at 2 and 4 months, indicating progressive hearing loss (Fig. ). ‖ 结论：(Fig. ) These results establish a novel noncanonical function of CXCR2 in neural excitability, extending beyond its well-characterized roles in immunity and inflammation.
局限
Consequently, heterozygous mice retain residual CXCR2 but still develop a deafness phenotype.；Notably, given the wide expression of CXCR2, the hearing loss observed in CXCR2+/− mice cannot completely exclude the potential contribution of CXCR2 deficiency in central auditory neurons; this is a notable limitation of this study.；The mechanisms underlying the CXCR2-mediated regulation of these structures warrant further investigation.
对本项目的价值
★☆☆☆☆ 脑老化是最大未满足需求，也是终点最难量化的领域；biomarker 与认知读数选择最敏感。
全文来源
PMC JATS 全文（正文 31,963 字符，已过标题/DOI 逐字归属校验）
原文题录
- 英文标题：CXCR2 deficiency impairs auditory function in spiral ganglion neurons by altering excitability.
- 期刊与标识：Cell Death Discov · PMID 42957635 · DOI 10.1038/s41420-026-03366-7
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。
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