Thyroid hormone-mediated autophagy and mitochondrial turnover in NAFLD

被引:50
|
作者
Sinha, Rohit Anthony [1 ]
Yen, Paul M. [1 ]
机构
[1] Duke NUS Grad Med Sch, Cardiovasc & Metab Disorders Program, Lab Hormonal Regulat, 8 Coll Rd, Singapore 169857, Singapore
来源
CELL AND BIOSCIENCE | 2016年 / 6卷
关键词
Autophagy; Liver; Mitophagy; NAFLD; Thyroid hormones; ULK1; NONALCOHOLIC FATTY LIVER; INSULIN-RESISTANCE; DISEASE; METABOLISM; AGONIST; RATS;
D O I
10.1186/s13578-016-0113-7
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
Non-alcoholic fatty liver disease (NAFLD) is a fast-growing silent epidemic that is present in both developed and developing countries. Initially thought as a benign deposition of lipids in the liver, it now has been shown to be a major risk factor for type II diabetes and one of the leading causes of cirrhosis. Recent findings suggest that dysregulation of mitochondrial homeostasis and autophagy play critical roles in the hepatocyte injury and insulin resistance of NAFLD. Thyroid hormone (TH) is a major stimulator of hepatic autophagy and mitochondrial function. Decreased TH action has been associated with NAFLD in man. In this review, we highlight some of the new discoveries that demonstrate the roles of TH in hepatic mitochondrial homeostasis via mitophagy and their implications for NAFLD.
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页数:6
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