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[老年性聋的发病机制与治疗。现状与未来展望]

[Pathogenesis and treatment of presbyacusis. Current status and future perspectives].

作者信息

Mazurek B, Stöver T, Haupt H, Gross J, Szczepek A

机构信息

HNO-Klinik und Poliklinik, Tinnituszentrum und Molekularbiologisches Forschungslabor, Charité - Universitätsmedizin Berlin, Campus Charité-Mitte, Charitéplatz 1, 10117 Berlin.

出版信息

HNO. 2008 Apr;56(4):429-32, 434-5. doi: 10.1007/s00106-008-1676-3.

Abstract

Factors responsible for presbyacusis include physiological ageing processes as well as endogenous or exogenous causes. In the industrial countries, two main exogenous causes are exposure to loud noise and obesity. Pathomechanisms contributing to presbyacusis are hypoxia/ischemia, reactive species formation and oxidative stress, apoptotic and necrotic death of hair cells and spiral ganglion cells as well as inherited and acquired mutations in the mitochondrial DNA. Important for the successful treatment of presbyacusis is a timely fitting of hearing aids on both ears to improve communication and provide the auditory system with acoustic information. Using the hearing aids will also elevate the detection threshold of an existing tinnitus signal. At present, several therapeutic strategies based on pharmacological intervention are under discussion. The application of antioxidants or caloric restriction are considered to prevent or reduce oxidative stress-induced damage. Animal experiments evidenced that superoxide dismutase 2 (SOD2) strongly decreases in age; thus, a further approach may be the overexpression or modulation of the SOD2 within the cochlea. Adenoviral-mediated gene transfer technology would be a tempting approach to address this type of therapy. Finally, hair cell regeneration could be a possible treatment of presbyacusis in the future.

摘要

导致老年性聋的因素包括生理衰老过程以及内源性或外源性原因。在工业化国家,两个主要的外源性原因是暴露于高强度噪声和肥胖。导致老年性聋的病理机制包括缺氧/缺血、活性物质形成和氧化应激、毛细胞和螺旋神经节细胞的凋亡和坏死性死亡以及线粒体DNA的遗传性和获得性突变。成功治疗老年性聋的关键是及时为双耳佩戴助听器,以改善沟通并为听觉系统提供声学信息。使用助听器还会提高现有耳鸣信号的检测阈值。目前,基于药物干预的几种治疗策略正在讨论中。应用抗氧化剂或热量限制被认为可以预防或减少氧化应激诱导的损伤。动物实验证明,超氧化物歧化酶2(SOD2)在衰老过程中会大幅减少;因此,另一种方法可能是在耳蜗内过表达或调节SOD2。腺病毒介导的基因转移技术将是实现这类治疗的诱人方法。最后,毛细胞再生可能是未来治疗老年性聋的一种方法。

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