The role of PARP1 in neurodegenerative diseases and aging

被引:80
|
作者
Mao, Kanmin [1 ,2 ]
Zhang, Guo [1 ,2 ]
机构
[1] Tongji Med Coll, Sch Publ Hlth, Dept Toxicol, Key Lab Environm Hlth,Minist Educ, Wuhan, Peoples R China
[2] Huazhong Univ Sci & Technol, Collaborat Innovat Ctr Brain Sci, Inst Brain Res, Wuhan, Peoples R China
基金
中国国家自然科学基金;
关键词
aging; DNA damage; neurodegenerative diseases; neuroinflammation; PARP1; OXIDATIVE STRESS; POLY(ADP-RIBOSE) POLYMERASE-1; INCREASED SUSCEPTIBILITY; METABOLIC-REGULATION; EXCISION-REPAIR; DAMAGE REPAIR; DNA; ACTIVATION; INHIBITION; NAD(+);
D O I
10.1111/febs.15716
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Neurodegenerative diseases, including Alzheimer's disease (AD) and Parkinson's disease (PD), are characterized by progressive memory loss and motor impairment. Aging is a major risk factor for neurodegenerative diseases. Neurodegenerative diseases and aging often develop in an irreversible manner and cause a significant socioeconomic burden. When considering their pathogenesis, many studies usually focus on mitochondrial dysfunction and DNA damage. More recently, neuroinflammation, autophagy dysregulation, and SIRT1 inactivation were shown to be involved in the pathogenesis of neurodegenerative diseases and aging. In addition, studies uncovered the role of poly (ADP-ribose)-polymerase-1 (PARP1) in neurodegenerative diseases and aging. PARP1 links to a cluster of stress signals, including those originated by inflammation and autophagy dysregulation. In this review, we summarized the recent research progresses on PARP1 in neurodegenerative diseases and aging, with an emphasis on the relationship among PARP1, neuroinflammation, mitochondria, and autophagy. We discussed the possibilities of treating neurodegenerative diseases and aging through targeting PARP1.
引用
收藏
页码:2013 / 2024
页数:12
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