The role of ER stress in lipid metabolism and lipotoxicity
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 stre...
| Main Authors: | , |
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| Format: | Article |
| Language: | English |
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Elsevier
2016-08-01
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| Series: | Journal of Lipid Research |
| Subjects: | |
| Online Access: | http://www.sciencedirect.com/science/article/pii/S002222752035207X |
| _version_ | 1818417808424304640 |
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| author | Jaeseok Han Randal J. Kaufman |
| author_facet | Jaeseok Han Randal J. Kaufman |
| author_sort | Jaeseok Han |
| collection | DOAJ |
| description | 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. |
| first_indexed | 2024-12-14T12:12:40Z |
| format | Article |
| id | doaj.art-a42c7d3160544609ac7b255c3b77aa4c |
| institution | Directory Open Access Journal |
| issn | 0022-2275 |
| language | English |
| last_indexed | 2024-12-14T12:12:40Z |
| publishDate | 2016-08-01 |
| publisher | Elsevier |
| record_format | Article |
| series | Journal of Lipid Research |
| spelling | doaj.art-a42c7d3160544609ac7b255c3b77aa4c2022-12-21T23:01:42ZengElsevierJournal of Lipid Research0022-22752016-08-0157813291338The role of ER stress in lipid metabolism and lipotoxicityJaeseok Han0Randal J. Kaufman1To whom correspondence should be addressed. (J.H.); (R.J. K.); Soonchunhyang Institute of Med-bio Science (SIMS),Soonchunhyang University, Cheonan-si, Choongchungnam-do, 31151, Republic of Korea; To whom correspondence should be addressed. (J.H.); (R.J. K.)To whom correspondence should be addressed. (J.H.); (R.J. K.); Degenerative Diseases Program,Sanford Burnham Prebys Medical Discovery Institute, La Jolla, CA 92307; To whom correspondence should be addressed. (J.H.); (R.J. K.)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.http://www.sciencedirect.com/science/article/pii/S002222752035207Xendoplasmic reticulumcell signalingdiabetesfatty acidlipids |
| spellingShingle | Jaeseok Han Randal J. Kaufman The role of ER stress in lipid metabolism and lipotoxicity Journal of Lipid Research endoplasmic reticulum cell signaling diabetes fatty acid lipids |
| title | The role of ER stress in lipid metabolism and lipotoxicity |
| title_full | The role of ER stress in lipid metabolism and lipotoxicity |
| title_fullStr | The role of ER stress in lipid metabolism and lipotoxicity |
| title_full_unstemmed | The role of ER stress in lipid metabolism and lipotoxicity |
| title_short | The role of ER stress in lipid metabolism and lipotoxicity |
| title_sort | role of er stress in lipid metabolism and lipotoxicity |
| topic | endoplasmic reticulum cell signaling diabetes fatty acid lipids |
| url | http://www.sciencedirect.com/science/article/pii/S002222752035207X |
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