Abstract
Alcoholic liver disease (ALD) is a globally prevalent chronic liver disease caused by chronic or binge consumption of alcohol. The liver is the major organ that metabolizes alcohol; therefore, it is particularly sensitive to alcohol intake. Metabolites and byproducts generated during alcohol metabolism cause liver damage, leading to ALD via several mechanisms, such as impairing lipid metabolism, intensifying inflammatory reactions, and inducing fibrosis. Despite the severity of ALD, the development of novel treatments has been hampered by the lack of animal models that fully mimic human ALD. To overcome the current limitations of ALD studies and therapy development, it is necessary to understand the molecular mechanisms underlying alcohol-induced liver injury. Hence, to provide insights into the progression of ALD, this review examines previous studies conducted on alcohol metabolism in the liver. There is a particular focus on the occurrence of ALD caused by hepatotoxicity originating from alcohol metabolism.
Highlights
Because there is a dearth of information about Alcoholic liver disease (ALD) pathogenesis exerted by non-oxidative ethanol metabolism, this section reviews the mechanisms underlying oxidative ethanol metabolite-mediated hepatotoxicity caused by excess alcohol exposure [45]
In human hepatic stellate cells (HSCs), protein kinase C (PKC) phosphorylates p70 S6 kinase (p70S6K) by activating extracellular signaling-regulated kinase (ERK) and phosphoinositide 3 kinase (PI3K), leading to collagen gene expression [84]. Another profibrogenic mechanism stimulated by acetaldehyde is the transforming growth factor beta (TGFβ) pathway, which is essential in liver fibrogenesis [85]
To reverse or inhibit the progression of ALD, identification of ALD risk factors and of mechanisms explaining their actions in ALD progression provides vital information for developing therapeutic targets for ALD
Summary
Publisher’s Note: MDPI stays neutral with regard to jurisdictional claims in published maps and institutional affiliations. In addition to social and psychiatric problems, more than 200 diseases that affect several organs, such as the brain, heart, gastrointestinal tract, and liver, are related to habitual alcohol consumption [6,7,8]. Among these alcoholdamaged organs, the liver is susceptible to damage because the liver is the primary site of alcohol metabolism in the body [9,10]. Understanding the process of alcohol metabolism in the liver and the actions of hepatotoxic intermediates involved in ALD progression could provide clues for developing ALD treatment strategies. The metabolic processes of alcohol are summarized, and ALD pathogenesis is reviewed, providing knowledge into the underlying mechanism of ALD
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