Thematic Review Series: Lipotoxicity: Many Roads to Cell Dysfunction and Cell Death The role of ER stress in lipid metabolism and lipotoxicity
- Authors
- Han, Jaeseok; Kaufman, Randal J.
- Issue Date
- Aug-2016
- Publisher
- Lipid Research, Inc.
- Keywords
- endoplasmic reticulum; cell signaling; diabetes; fatty acid; lipids
- Citation
- Journal of Lipid Research, v.57, no.8, pp 1329 - 1338
- Pages
- 10
- Journal Title
- Journal of Lipid Research
- Volume
- 57
- Number
- 8
- Start Page
- 1329
- End Page
- 1338
- URI
- https://scholarworks.bwise.kr/sch/handle/2021.sw.sch/8914
- DOI
- 10.1194/jlr.R067595
- ISSN
- 0022-2275
1539-7262
- Abstract
- 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.
- Files in This Item
- There are no files associated with this item.
- Appears in
Collections - Graduate School > Department of Integrated Biomedical Science > 1. Journal Articles
Items in ScholarWorks are protected by copyright, with all rights reserved, unless otherwise indicated.