期刊
JOURNAL OF GASTROENTEROLOGY AND HEPATOLOGY
卷 32, 期 5, 页码 981-991出版社
WILEY
DOI: 10.1111/jgh.13619
关键词
ER stress; liver disease; miRNA; RIDD; stress mediated toxicity
资金
- National Research Foundation of Korea, Republic of Korea [2008-0062279, 2015R1A2A1A13001849]
- National Research Foundation of Korea [2015R1A2A1A13001849] Funding Source: Korea Institute of Science & Technology Information (KISTI), National Science & Technology Information Service (NTIS)
Compromised protein folding capacity in the endoplasmic reticulum (ER) leads to a protein traffic jam that produces a toxic environment called ER stress. However, the ER smartly handles such a critical situation by activating a cascade of proteins responsible for sensing and responding to the noxious stimuli of accumulated proteins. The ER protein load is higher in secretory cells, such as liver hepatocytes, which are thus prone to stress-mediated toxicity and various diseases, including alcohol-induced liver injury, fatty liver disease, and viral hepatitis. Therefore, we discuss the molecular cues that connect ER stress to hepatic diseases. Moreover, we review the literature on ER stress-regulated miRNA in the pathogenesis of liver diseases to give a comprehensive overview of mechanistic insights connecting ER stress and miRNA in the context of liver diseases. We also discuss currently discovered regulated IRE1 dependent decay in regulation of hepatic diseases.
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