Peroxisome quality control and dysregulated lipid metabolism in neurodegenerative diseases

被引:72
作者
Jo, Doo Sin [1 ]
Park, Na Yeon [2 ]
Cho, Dong-Hyung [1 ,2 ]
机构
[1] Kyungpook Natl Univ, Brain Sci & Engn Inst, Daegu 41566, South Korea
[2] Kyungpook Natl Univ, Sch Life Sci, Daegu 41566, South Korea
基金
新加坡国家研究基金会;
关键词
ALZHEIMERS-DISEASE; DOCOSAHEXAENOIC ACID; AUTOPHAGIC DEGRADATION; PARKINSONS-DISEASE; TARGETING SIGNAL; OXIDATIVE STRESS; AMYLOID-BETA; CHOLESTEROL-METABOLISM; MAMMALIAN PEROXISOMES; MOLECULAR-MECHANISM;
D O I
10.1038/s12276-020-00503-9
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
In recent decades, the role of the peroxisome in physiology and disease conditions has become increasingly important. Together with the mitochondria and other cellular organelles, peroxisomes support key metabolic platforms for the oxidation of various fatty acids and regulate redox conditions. In addition, peroxisomes contribute to the biosynthesis of essential lipid molecules, such as bile acid, cholesterol, docosahexaenoic acid, and plasmalogen. Therefore, the quality control mechanisms that regulate peroxisome biogenesis and degradation are important for cellular homeostasis. Current evidence indicates that peroxisomal function is often reduced or dysregulated in various human disease conditions, such as neurodegenerative diseases. Here, we review the recent progress that has been made toward understanding the quality control systems that regulate peroxisomes and their pathological implications.
引用
收藏
页码:1486 / 1495
页数:10
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