New Insights into the Pathogenesis of Alcohol-Induced ER Stress and Liver Diseases
Alcohol-induced liver disease increasingly contributes to human mortality worldwide. Alcohol-induced endoplasmic reticulum (ER) stress and disruption of cellular protein homeostasis have recently been established as a significant mechanism contributing to liver diseases. The alcohol-induced ER stres...
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| Format: | Article |
| Language: | English |
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Wiley
2014-01-01
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| Series: | International Journal of Hepatology |
| Online Access: | http://dx.doi.org/10.1155/2014/513787 |
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| author | Cheng Ji |
| author_facet | Cheng Ji |
| author_sort | Cheng Ji |
| collection | DOAJ |
| description | Alcohol-induced liver disease increasingly contributes to human mortality worldwide. Alcohol-induced endoplasmic reticulum (ER) stress and disruption of cellular protein homeostasis have recently been established as a significant mechanism contributing to liver diseases. The alcohol-induced ER stress occurs not only in cultured hepatocytes but also in vivo in the livers of several species including mouse, rat, minipigs, zebrafish, and humans. Identified causes for the ER stress include acetaldehyde, oxidative stress, impaired one carbon metabolism, toxic lipid species, insulin resistance, disrupted calcium homeostasis, and aberrant epigenetic modifications. Importance of each of the causes in alcohol-induced liver injury depends on doses, duration and patterns of alcohol exposure, genetic disposition, environmental factors, cross-talks with other pathogenic pathways, and stages of liver disease. The ER stress may occur more or less all the time during alcohol consumption, which interferes with hepatic protein homeostasis, proliferation, and cell cycle progression promoting development of advanced liver diseases. Emerging evidence indicates that long-term alcohol consumption and ER stress may directly be involved in hepatocellular carcinogenesis (HCC). Dissecting ER stress signaling pathways leading to tumorigenesis will uncover potential therapeutic targets for intervention and treatment of human alcoholics with liver cancer. |
| format | Article |
| id | doaj-art-88cd03f3e54e44c0a6f1bbffe5376c72 |
| institution | Kabale University |
| issn | 2090-3448 2090-3456 |
| language | English |
| publishDate | 2014-01-01 |
| publisher | Wiley |
| record_format | Article |
| series | International Journal of Hepatology |
| spelling | doaj-art-88cd03f3e54e44c0a6f1bbffe5376c722025-08-20T03:38:05ZengWileyInternational Journal of Hepatology2090-34482090-34562014-01-01201410.1155/2014/513787513787New Insights into the Pathogenesis of Alcohol-Induced ER Stress and Liver DiseasesCheng Ji0USC Research Center for Liver Disease, Department of Medicine, Keck School of Medicine of USC, University of Southern California, 2011 Zonal Avenue, HMR-101, Los Angeles, CA 90089, USAAlcohol-induced liver disease increasingly contributes to human mortality worldwide. Alcohol-induced endoplasmic reticulum (ER) stress and disruption of cellular protein homeostasis have recently been established as a significant mechanism contributing to liver diseases. The alcohol-induced ER stress occurs not only in cultured hepatocytes but also in vivo in the livers of several species including mouse, rat, minipigs, zebrafish, and humans. Identified causes for the ER stress include acetaldehyde, oxidative stress, impaired one carbon metabolism, toxic lipid species, insulin resistance, disrupted calcium homeostasis, and aberrant epigenetic modifications. Importance of each of the causes in alcohol-induced liver injury depends on doses, duration and patterns of alcohol exposure, genetic disposition, environmental factors, cross-talks with other pathogenic pathways, and stages of liver disease. The ER stress may occur more or less all the time during alcohol consumption, which interferes with hepatic protein homeostasis, proliferation, and cell cycle progression promoting development of advanced liver diseases. Emerging evidence indicates that long-term alcohol consumption and ER stress may directly be involved in hepatocellular carcinogenesis (HCC). Dissecting ER stress signaling pathways leading to tumorigenesis will uncover potential therapeutic targets for intervention and treatment of human alcoholics with liver cancer.http://dx.doi.org/10.1155/2014/513787 |
| spellingShingle | Cheng Ji New Insights into the Pathogenesis of Alcohol-Induced ER Stress and Liver Diseases International Journal of Hepatology |
| title | New Insights into the Pathogenesis of Alcohol-Induced ER Stress and Liver Diseases |
| title_full | New Insights into the Pathogenesis of Alcohol-Induced ER Stress and Liver Diseases |
| title_fullStr | New Insights into the Pathogenesis of Alcohol-Induced ER Stress and Liver Diseases |
| title_full_unstemmed | New Insights into the Pathogenesis of Alcohol-Induced ER Stress and Liver Diseases |
| title_short | New Insights into the Pathogenesis of Alcohol-Induced ER Stress and Liver Diseases |
| title_sort | new insights into the pathogenesis of alcohol induced er stress and liver diseases |
| url | http://dx.doi.org/10.1155/2014/513787 |
| work_keys_str_mv | AT chengji newinsightsintothepathogenesisofalcoholinducederstressandliverdiseases |