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The role of ER stress in lipid metabolism and lipotoxicity
Open accessAbstract
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.
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Clapham, D. E. (2007) · Cell · doi:10.1016/j.cell.2007.11.028 · Cited by 4,175
Protein misfolding in the endoplasmic reticulum as a conduit to human disease
Wang, M., & Kaufman, R. J. (2016) · Nature · doi:10.1038/nature17041 · Cited by 1,630
Self-citationTLR activation of the transcription factor XBP1 regulates innate immune responses in macrophages
Martinon, F., Chen, X., Lee, A.-H., & Glimcher, L. H. (2010) · Nature Immunology · doi:10.1038/ni.1857 · Cited by 996
Kammoun, H. L., Chabanon, H., Hainault, I., Luquet, S., Magnan, C., Koike, T., Ferré, P., & Foufelle, F. (2009) · Journal of Clinical Investigation · doi:10.1172/jci37007 · Cited by 732
Gluttony, sloth and the metabolic syndrome: a roadmap to lipotoxicity
Unger, R. H., & Scherer, P. E. (2010) · Trends in Endocrinology & Metabolism · doi:10.1016/j.tem.2010.01.009 · Cited by 436
Ao, N., Yang, J., Wang, X., & Du, J. (2016) · Hepatology Research · doi:10.1111/hepr.12551 · Cited by 56
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Broadfield, L. A., Pane, A. A., Talebi, A., Swinnen, J. V., & Fendt, S.-M. (2021) · Developmental Cell · doi:10.1016/j.devcel.2021.04.013 · Cited by 758
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Zadoorian, A., Du, X., & Yang, H. (2023) · Nature Reviews Endocrinology · doi:10.1038/s41574-023-00845-0 · Cited by 617
Arroyave-Ospina, J. C., Wu, Z., Geng, Y., & Moshage, H. (2021) · Antioxidants · doi:10.3390/antiox10020174 · Cited by 527
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Zhao, Q., Liu, J., Deng, H., Ma, R., Liao, J.-Y., Liang, H., Hu, J., Li, J., Guo, Z., Cai, J., et al. (2020) · Cell · doi:10.1016/j.cell.2020.08.009 · Cited by 469
Metadata
- Authors
- Han, J., & Kaufman, R. J.
- Venue
- Journal of Lipid Research
- Publisher
- Elsevier BV
- Published
- 2016-08
- Volume
- 57
- Issue
- 8
- Pages
- 1329-1338
- ISSN
- 0022-2275 (ISSN-L)
- OpenAlex
- W2345368448
- Cited by
- 645
- References
- 6
- FWCI
- 23.66
- Type
- journal article
- Language
- en
- Open access
- hybrid
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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
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