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The role of HDAC11 in age-related hearing loss: Mechanisms and therapeutic implications.
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Department of Otorhinolaryngology Head and Neck Surgery, The First Affiliated Hospital of Nanchang University, 17 Yongwai Zhengjie, Donghu District, Nanchang City, Jiangxi Province, 330000, China.
This study focuses on the critical role of HDAC11 in age-related hearing loss and its underlying mechanisms. Through cellular experiments, we deeply explored the effects of HDAC11 on the proliferation and senescence of HEI-OC1 cells. The results showed that HDAC11 overexpression significantly reduced the acetylation level of α-microtubule protein, which in turn affected the stability of microtubule structure and accelerated the apoptosis and senescence process of HEI-OC1 cells.
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The therapeutic potential of HDAC inhibitors containing a hydroxamic acid moiety as a zinc-binding group (ZBG) is limited in clinical use due to their potential mutagenicity. In addition, hydroxamic acids often exhibit off-target effects that can lead to undesirable toxicity. Therefore, the development of HDAC inhibitors with alternative ZBGs has proven to be a promising approach to overcome these drawbacks.
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Age-related macular degeneration (AMD) is a top cause of severe vision loss and blindness in older adults globally. This multifactorial disease arises from genetic, environmental, and age-related factors. Protein acetylation modification plays a key role in AMD progression through both epigenetic and non-epigenetic pathways.
View Article and Find Full Text PDFBackground: Histone deacetylase 11 (HDAC11) is the sole member of class IV HDACs, implicated in tumor growth, immune regulation, and oxidative stress injury. Its specific role in renal fibrosis and underlying mechanisms remains unclear.
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