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Alcoholic liver disease (ALD) is a major cause of liver-related morbidity and mortality worldwide.1 Although the most effective therapy for patients with ALD is alcohol cessation, targeted therapies are needed in patients with progressive disease and active drinking, and for those with life-threatening conditions such as alcoholic hepatitis. The development of such therapies is hampered by poor knowledge of the main disease drivers. During the last two decades, the cellular and molecular mechanisms of the hepatic wound-healing response to repeated exposure to alcohol have been partially delineated. ALD is characterised by steatosis, inflammatory infiltrate mainly composed of polymorphonuclear cells, hepatocellular injury and progressive fibrosis. The cellular and molecular basis includes paracrine stimulation by damaged hepatocytes, the innate immune system, oxidative stress and the resulting activation of non-parenchymal cells. Several inflammatory and fibrogenic mediators are released at the areas of tissue repair and perpetuate inflammation, leading to progressive fibrosis and organ failure. Among these mediators, a growing body of evidence indicates that endogenous cannabinoids have an important role in hepatic wound healing and represent promising druggable targets for therapy.2
The endocannabinoid system is composed of endocannabinoids (anandamide (AEA), 2-arachidonoyl glycerol (2-AG)), cannabinoid receptors (CB) (CB1 and CB2), and the enzymes involved in endocannabinoid biosynthesis and degradation.2 The degradation enzymes include fatty acid amide hydrolase and monoglyceride lipase for degradation of AEA and 2-AG, respectively. CB1 receptors are expressed at high …
Contributors Both authors contributed equally to revise the original paper by Kim et al, to write the commentary and approved the final version of our manuscript.
Competing interests None.
Provenance and peer review Commissioned; externally peer reviewed.
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