[3-9]NAD+ deficiency is a common central pathological factor of a number of diseases and aging: Mechanisms and therapeutic implications

发布者:系统管理员发布时间:2018-03-09浏览次数:1096

 

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 :殷卫海教授(上海交通大学Med-X研究院副院长、生物医学工程学院特聘教授、中国城市治理研究院研究员)

 

报告时间2018313日(周二),14:00

 

报告地点:独墅湖校区二期药学院云轩楼2301会议室

 

报告人简介

        殷卫海教授1985年毕业于上海医科大学(现复旦大学上海医学院)于上海交大联合建立的生物医学工程专业。他于2002-2008在国际顶级医学院——美国UCSF神经科学领域担任PI。在PNAS等国际科学杂志上发表了近90篇论文(大多数为通讯作者或第一作者),被引用超过4600次(Google Scholar)。他是国际上“NAD+耗竭是疾病和老化的一个核心共同机制这一理论的提出者以及这一领域的开创者。作为客座主编,主编了三个SCI杂志(IF>3.5)专辑。回国后担任了“973”项目子课题、上海全球创新中心优先启动计划重大项目子课题、国家自然科学基金、浦江人才计划等一系列基金的PI 担任了“973”基金评委、国家自然科学基金评委、美国心脏协会基金评委。近年来殷教授担任了上海主要的有关医学大数据的科研基金脑卒中领域的主要科学家。在无创检测重大疾病方面,殷教授递交了38项国家或国际发明专利申请。他的科学发现曾被美联社、BBC和《科技日报》等主要媒体介绍。

 

报告摘要

 

Increasing evidence has indicated critical roles of NAD+ in various biological functions. NAD+ deficiency has been found in models of a number of diseases such as cerebral ischemia, myocardial ischemia and diabetes, and in models of aging.  Application of NAD+ or other approaches that can restore NAD+ levels are highly protective in these models of diseases and aging. NAD+ produces its beneficial effects by targeting at multiple pathological pathways, including attenuating mitochondrial alterations, DNA damage and oxidative stress by modulating such enzymes as sirtuins, glyceraldehyde-3-phosphate dehydrogenase and AP endonuclease. These findings have suggested great therapeutic and nutritional potential of NAD+ for diseases and senescence. Approaches that can restore NAD+ levels are highly protective in the models of such diseases as glaucoma.  The NAD+ deficiency in the diseases and aging results from not only poly(ADP-ribose) polymerase-1 (PARP-1) activation, but also decreased Nicotinamide phosphoribosyltransferase (Nampt) activity and increased CD38 activity.  Significant biological effects of extracellular NAD+ have been found. Increasing evidence has suggested that NAD+ deficiency is a common central pathological factor in a number of diseases and aging. Future studies are required for solidly establishing the concept that ‘NAD+ deficiency is a common central pathological factor in a number of disease and aging’. It is also necessary to further investigate the mechanisms underlying the NAD+ deficiency in the diseases and aging. Preclinical and clinical studies should be conducted to determine the therapeutic potential of NAD+ for the diseases and aging.