The DOI matches its Crossref record; 11 of the 11 references it cites were found in a registry or an index.
The contribution of endoplasmic reticulum stress to liver diseases
Open accessAbstract
The unfolded protein response (UPR) is an evolutionarily conserved cell signaling pathway that is activated to regulate protein synthesis and restore homeostatic equilibrium when the cell is stressed from increased client protein load or the accumulation of unfolded or malfolded proteins. Once activated, this signaling pathway can either result in the recovery of homeostasis or can activate a cascade of events that ultimately result in cell death. The UPR/endoplasmic reticulum (ER) stress response spectrum and its interplay with other cellular organelles play an important role in the pathogenesis of disease in secretory cells rich in ER, such as hepatocytes. Over the past 2 decades, the contribution of ER stress to various forms of liver diseases has been examined. Robust support for a contributing, as opposed to a secondary role, for ER stress response is seen in the nonalcoholic steatohepatitis, alcoholic liver disease, ischemia/reperfusion injury, and cholestatic models of liver disease. The exact direction of the cause and effect relationship between modes of cell injury and ER stress remains elusive. It is apparent that a complex interplay exists between ER stress response, conditions that promote it, and those that result from it. A vicious cycle in which ER stress promotes inflammation, cell injury, and steatosis and in which steatogenesis, inflammation, and cell injury aggravate ER stress seems to be at play. It is perhaps the nature of such a vicious cycle that is the key pathophysiologic concept. Therapeutic approaches aimed at interrupting the cycle may dampen the stress response and the ensuing injury. (hepatology 2011;)
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CSH guidelines for the diagnosis and treatment of drug-induced liver injury
Drug-induced Liver Injury (DILI) Study Group, Yu, Y.-C., Chinese Society of Hepatology (CSH), Chinese Medical Association (CMA), Mao, Y.-M., Chen, C.-W., Chen, J.-J., Chen, J., Cong, W.-M., Ding, Y., et al. (2017) · Hepatology International · doi:10.1007/s12072-017-9793-2 · Cited by 254
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Metadata
- Authors
- Dara, L., Ji, C., & Kaplowitz, N.
- Venue
- Hepatology
- Published
- 2011-05
- Volume
- 53
- Issue
- 5
- Pages
- 1752-1763
- ISSN
- 0270-9139 (ISSN-L)
- OpenAlex
- W1966625828
- Cited by
- 371
- References
- 11
- FWCI
- 10.21
- Type
- journal article
- Language
- en
- Open access
- green
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