期刊
JOURNAL OF LIPID RESEARCH
卷 57, 期 8, 页码 1329-1338出版社
ELSEVIER
DOI: 10.1194/jlr.R067595
关键词
endoplasmic reticulum; cell signaling; diabetes; fatty acid; lipids
资金
- Office of Extramural Research, National Institutes of Health [DK042394, DK088227, DK103183, CA128814]
- Basic Science Research Program through National Research Foundation of Korea - Ministry of Education [NRF-2015R1D1A1A01058846]
- Soonchunhyang University Research Fund
The endoplasmic reticulum (ER) is a cellular organelle important for regulating calcium homeostasis, lipid metabolism, protein synthesis, and posttranslational modification and trafficking. Numerous environmental, physiological, and pathological insults disturb ER homeostasis, referred to as ER stress, in which a collection of conserved intracellular signaling pathways, termed the unfolded protein response (UPR), are activated to maintain ER function for cell survival. However, excessive and/or prolonged UPR activation leads to initiation of self-destruction through apoptosis. Excessive accumulation of lipids and their intermediate products causes metabolic abnormalities and cell death, called lipotoxicity, in peripheral organs, including the pancreatic islets, liver, muscle, and heart. Because accumulating evidence links chronic ER stress and defects in UPR signaling to lipotoxicity in peripheral tissues, understanding the role of ER stress in cell physiology is a topic under intense investigation. In this review, we highlight recent findings that link ER stress and UPR signaling to the pathogenesis of peripheral organs due to lipotoxicity.-Han, J., and R. J. Kaufman. The role of ER stress in lipid metabolism and lipotoxicity.
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