Autophagy function and its relationship to pathology, clinical applications, drug metabolism and toxicity

被引:47
作者
Petibone, Dayton M. [1 ]
Majeed, Waqar [2 ]
Casciano, Daniel A. [2 ]
机构
[1] US FDA, Natl Ctr Toxicol Res, Div Genet & Mol Toxicol, Jefferson, AR 72079 USA
[2] Univ Arkansas, Ctr Integrat Nanotechnol Sci, Little Rock, AR 72204 USA
关键词
autophagy; drug toxicity; amphiphilic cationic drugs; phospholipidosis; disease progression; carcinogenesis; clinical applications; POTENT HEPATOCARCINOGEN METHAPYRILENE; ESOPHAGEAL CANCER-CELLS; TUMOR-SUPPRESSOR GENE; BECLIN; EXPRESSION; CISPLATIN RESISTANCE; REGULATES AUTOPHAGY; NEURODEGENERATIVE DISEASE; INDUCED PHOSPHOLIPIDOSIS; RHEUMATOID-ARTHRITIS; MOLECULAR-MECHANISMS;
D O I
10.1002/jat.3393
中图分类号
R99 [毒物学(毒理学)];
学科分类号
100405 ;
摘要
Autophagy is a cellular process that facilitates nutrient turnover and removal of expended macromolecules and organelles to maintain homeostasis. The recycling of cytosolic macromolecules and damaged organelles by autophagosomes occurs through the lysosomal degradation pathway. Autophagy can also be upregulated as a prosurvival pathway in response to stress stimuli such as starvation, hypoxia or cell damage. Over the last two decades, there has been a surge in research revealing the basic molecular mechanisms of autophagy in mammalian cells. A corollary of an advanced understanding of autophagy has been a concurrent expansion of research into understanding autophagic function and dysfunction in pathology. Recent studies have revealed a pivotal role for autophagy in drug toxicity, and for utilizing autophagic components as diagnostic markers and therapeutic targets in treating disease and cancer. In this review, advances in understanding the molecular basis of mammalian autophagy, methods used to induce and evaluate autophagy, and the diverse interactions between autophagy and drug toxicity, disease progression and carcinogenesis are discussed. Copyright (c) 2016 John Wiley & Sons, Ltd.
引用
收藏
页码:23 / 37
页数:15
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