【摘 要】
：
Age-related hearing loss (ARHL) is a predominant neurodegenerative disease with age.Here, we demonstrate for the first time that, in the aging process, the levels and activities of SIRT1 and SIRT3 are
【机 构】
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Wonkwang University School of Medicine South Korea
【出 处】
：
BIT`s 3rd Annual World Congress of NeuroTalk-2012(2012第三届国际神
论文部分内容阅读
Age-related hearing loss (ARHL) is a predominant neurodegenerative disease with age.Here, we demonstrate for the first time that, in the aging process, the levels and activities of SIRT1 and SIRT3 are suppressed by reduction of intracellular NAD+ levels.We provide evidence that the decline in SIRT1 and SIRT3 levels aggravates ARHL by increasing acetylation of NF-B and p53, suggesting ARHL may occur through the induction of inflammatory responses and oxidative stress as well as the mitochondrial dysfunctions, playing an essential role for the apoptotic cell death in cochlear tissues.Moreover, we show that the simultaneous induction of the cytosolic and mitochondrial NAD+ levels using β-lapachone, whose intracellular target is NQO-1, prevents mice from ARHL and its deleterious effects through the maintenance of the mitochondrial structure and function.These results suggest that direct modulation of the cellular NAD+ level by pharmacological agents could be a promising option for treating ARHL.
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