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<p>Lipid metabolism is an important biological process that maintains the dynamic balance of several key functions, such as intracellular energy metabolism, signal transduction, and membrane remodeling. However, the role of lipid metabolism in auditory function and the underlying mechanisms remain unclear. Our results reveal that the neomycin exposure disrupts lipid metabolism in auditory system. We find that neomycin-induced hair cells (HC) damage leads to abnormal lipid droplets (LD) accumulation. Further research reveals that decreased YAP expression is a key factor that contributes to abnormal LD accumulation. In both in vivo and in vitro studies, <i>Yap</i> overexpression reduces abnormal LD accumulation and mitigated HC damage. To further investigate its downstream mechanisms, we perform a cross-analysis of <i>Yap</i>-related and lipid metabolism–related genes, identifying that <i>Cox2</i> is a key downstream target of <i>Yap</i> that contributes to LD accumulation and HC damage. Our work provides clear evidence for the role of lipid metabolism in neomycin-induced hearing loss and elucidates underlying mechanism of <i>Yap/Cox2</i> pathway. These findings provide new perspectives and avenues for the clinical treatment of sensorineural hearing loss.</p>

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Regulation of lipid droplets accumulation by the Hippo–YAP/COX2 signaling pathway in neomycin-induced ototoxicity

  • 期刊论文

  • 出版模式：

    开放获取

  • 发表日期：

    2026年4月16日

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  • Wenli Hao,
  • Song Gao,
  • Suhan Guo,
  • Jingjing Luo,
  • Siyu Li,
  • Junze Lu,
  • Lulu Jiang,
  • Jie Lu,
  • Nan Wang,
  • Aijia Ran,
  • Xiaoyun Qian,
  • Xia Gao,
  • Chenjie Yu,
  • Cheng Cheng

摘要

Lipid metabolism is an important biological process that maintains the dynamic balance of several key functions, such as intracellular energy metabolism, signal transduction, and membrane remodeling. However, the role of lipid metabolism in auditory function and the underlying mechanisms remain unclear. Our results reveal that the neomycin exposure disrupts lipid metabolism in auditory system. We find that neomycin-induced hair cells (HC) damage leads to abnormal lipid droplets (LD) accumulation. Further research reveals that decreased YAP expression is a key factor that contributes to abnormal LD accumulation. In both in vivo and in vitro studies, Yap overexpression reduces abnormal LD accumulation and mitigated HC damage. To further investigate its downstream mechanisms, we perform a cross-analysis of Yap-related and lipid metabolism–related genes, identifying that Cox2 is a key downstream target of Yap that contributes to LD accumulation and HC damage. Our work provides clear evidence for the role of lipid metabolism in neomycin-induced hearing loss and elucidates underlying mechanism of Yap/Cox2 pathway. These findings provide new perspectives and avenues for the clinical treatment of sensorineural hearing loss.