Shared molecular and cellular mechanisms of premature ageing and ageing-associated diseases

被引：233

作者：

Kubben, Nard ^{[1
]}

Misteli, Tom ^{[1
]}

机构：

[1] NCI, NIH, Bethesda, MD 20892 USA

来源：

NATURE REVIEWS MOLECULAR CELL BIOLOGY | 2017年 / 18卷 / 10期

关键词：

GILFORD-PROGERIA-SYNDROME; CHRONIC KIDNEY-DISEASE; NF-KAPPA-B; IDIOPATHIC PULMONARY-FIBROSIS; BASE EXCISION-REPAIR; DEFECTIVE-DNA REPAIR; A-TYPE LAMINS; ALZHEIMERS-DISEASE; LIFE-SPAN; WERNER SYNDROME;

D O I：

10.1038/nrm.2017.68

中图分类号：

Q2 [细胞生物学];

学科分类号：

071009 ; 090102 ;

摘要：

Ageing is the predominant risk factor for many common diseases. Human premature ageing diseases are powerful model systems to identify and characterize cellular mechanisms that underpin physiological ageing. Their study also leads to a better understanding of the causes, drivers and potential therapeutic strategies of common diseases associated with ageing, including neurological disorders, diabetes, cardiovascular diseases and cancer. Using the rare premature ageing disorder Hutchinson-Gilford progeria syndrome as a paradigm, we discuss here the shared mechanisms between premature ageing and ageing-associated diseases, including defects in genetic, epigenetic and metabolic pathways; mitochondrial and protein homeostasis; cell cycle; and stem cell-regenerative capacity.

引用

收藏

页码：595 / 609

页数：15

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