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2021
DOI: 10.35946/arcr.v41.1.12
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Hepatic Cannabinoid Signaling in the Regulation of Alcohol-Associated Liver Disease

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Cited by 7 publications
(9 citation statements)
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“…Thirdly, paracetamol and cannabinoids have several intense interactions with difficult-to-judge clinical importance. Finally, there are suggestions of cannabinoids contributing to nonalcoholic liver disease, fibrosis, and inflammation, but the data are conflicting and inconclusive [298,299].…”
Section: Liver Effects In the Context Of Cannabinoid Usementioning
confidence: 99%
“…Thirdly, paracetamol and cannabinoids have several intense interactions with difficult-to-judge clinical importance. Finally, there are suggestions of cannabinoids contributing to nonalcoholic liver disease, fibrosis, and inflammation, but the data are conflicting and inconclusive [298,299].…”
Section: Liver Effects In the Context Of Cannabinoid Usementioning
confidence: 99%
“…Similar to NAFLD, ALD also comprises symptoms including liver injury accompanied by simple steatosis or steatohepatitis, which can progress to liver cirrhosis and HCC [ 24 ]. Indeed, as for HFD, excessive and chronic alcohol consumption causes hepatic immune disturbances, and the excessive activation of inflammatory caspases in proinflammatory Kupffer cells, resulting in pyroptosis with the secretion of inflammatory cytokines, and oxidative stress with the production of ROS, and it is accompanied by the metabolic dysfunction of hepatocytes and abnormal lipogenesis, which leads to hepatic steatosis [ 4 , 24 ]. Given the underlying similarities in ALD and NAFLD/NASH pathogenesis, it is not surprising that alcohol intake can also induce changes in the eCBS [ 71 ].…”
Section: The Endocannabinoid System In Chronic Liver Diseasesmentioning
confidence: 99%
“…Treating alcohol-fed mice with CBD inhibited the activation of NLRP3 inflammasome, reduced the pyroptosis and liver inflammation, and protected the mice livers against steatohepatitis [ 34 ]. Accordingly, these findings suggest that, by activating hepatic CB1R, chronic alcohol intake stimulates the secretion of 2-AG by activated HSCs, which, in turn, promotes hepatic lipogenesis, on the one hand, and, on the other hand, inhibits fatty acid oxidation, thereby creating a disbalance between lipogenesis and lipid oxidation and resulting in chronic fat accumulation in the liver and steatosis [ 4 , 71 , 72 , 73 ]. Moreover, the activation of the hepatic CB1R by excessive alcohol intake also drives the activation of the key processing pathways involved in the setting of alcohol-induced steatohepatitis and liver inflammation [ 34 ].…”
Section: The Endocannabinoid System In Chronic Liver Diseasesmentioning
confidence: 99%
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“… 29 In their review of the mechanisms of cannabinoid receptor signaling in hepatic pathogenesis, Yang, Choi, and Jeong summarize evidence in support of cannabinoid-based treatments for alcohol-associated liver disease. 30 Lees, Debenham, and Squeglia present a comprehensive overview of longitudinal neuropsychological and neuroimaging studies on the independent and combined effects of cannabis and alcohol use on the developing human brain. 31 Several articles review findings on the impact of cannabis use on alcohol consumption and consequences, and how this association may differ by cannabis formulation or by user characteristics, 32 with a specific focus on simultaneous alcohol and cannabis use, and contextual characteristics of co-use in young adults.…”
mentioning
confidence: 99%