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<p>SIRT3 protects against metabolic stress-induced cellular damage by regulating mitochondrial homeostasis and autophagy-related pathways in various tissues. It has also been implicated in protecting cochlear hair cells and synapses after noise exposure. However, whether protection associated with SIRT3 modulation in noise-induced hearing loss (NIHL) is accompanied by autophagy-related changes remains unclear. Here, we found that AAV-SIRT3 delivery was associated with reduced LC3B level and increased p62 accumulation in the noise-exposed cochlea, suggesting attenuation of noise-associated autophagy-related marker changes. AAV-SIRT3 delivery was also associated with reduced 4-HNE accumulation, partial preservation of mitochondrial membrane potential, and a decreased Ac-SOD2/SOD2 ratio. These findings suggest that AAV-SIRT3-associated protection against NIHL is accompanied by reduced mitochondrial oxidative injury and attenuation of autophagy-related cochlear stress responses.</p>

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AAV-SIRT3 delivery protects against noise-induced hearing loss in association with reduced oxidative injury and autophagy-related changes

  • 期刊论文

  • 出版模式：

    开放获取

  • 发表日期：

    2026年7月13日

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  • Ting Zhang,
  • Wenqi Liang,
  • Shusheng Gong

摘要

SIRT3 protects against metabolic stress-induced cellular damage by regulating mitochondrial homeostasis and autophagy-related pathways in various tissues. It has also been implicated in protecting cochlear hair cells and synapses after noise exposure. However, whether protection associated with SIRT3 modulation in noise-induced hearing loss (NIHL) is accompanied by autophagy-related changes remains unclear. Here, we found that AAV-SIRT3 delivery was associated with reduced LC3B level and increased p62 accumulation in the noise-exposed cochlea, suggesting attenuation of noise-associated autophagy-related marker changes. AAV-SIRT3 delivery was also associated with reduced 4-HNE accumulation, partial preservation of mitochondrial membrane potential, and a decreased Ac-SOD2/SOD2 ratio. These findings suggest that AAV-SIRT3-associated protection against NIHL is accompanied by reduced mitochondrial oxidative injury and attenuation of autophagy-related cochlear stress responses.