Nucleophagy: from homeostasis to disease

被引:79
|
作者
Papandreou, Margarita-Elena [1 ,2 ]
Tavernarakis, Nektarios [1 ,2 ]
机构
[1] Fdn Res & Technol Hellas, Inst Mol Biol & Biotechnol, Iraklion 71110, Crete, Greece
[2] Univ Crete, Sch Med, Dept Basic Sci, Iraklion 71110, Crete, Greece
来源
CELL DEATH AND DIFFERENTIATION | 2019年 / 26卷 / 04期
基金
欧洲研究理事会;
关键词
LIFE-SPAN EXTENSION; PIECEMEAL MICROAUTOPHAGY; AUTOPHAGY DEGRADES; NUCLEAR-STRUCTURE; CELL-DEATH; RECEPTOR; AGE; DEGRADATION; MECHANISMS; HUNTINGTIN;
D O I
10.1038/s41418-018-0266-5
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
Nuclear abnormalities are prominent in degenerative disease and progeria syndromes. Selective autophagy of organelles is instrumental in maintaining cell homeostasis and prevention of premature ageing. Although the nucleus is the control centre of the cell by safeguarding our genetic material and controlling gene expression, little is known in relation to nuclear autophagy. Here we present recent discoveries in nuclear recycling, namely nucleophagy in physiology in yeast and nucleophagic events that occur in pathological conditions in mammals. The selective nature of degrading nuclear envelope components, DNA, RNA and nucleoli is highlighted. Potential effects of perturbed nucleophagy in senescence and longevity are examined. Moreover, the open questions that remain to be explored are discussed concerning the conditions, receptors and substrates in homeostatic nucleophagy.
引用
收藏
页码:630 / 639
页数:10
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