Abstract
Alcoholic liver disease (ALD) is characterized by the injury, inflammation, and scarring in the liver owing to excessive alcohol consumption. Currently, ALD is a leading cause for liver transplantation. Therefore, extensive studies (in vitro, in experimental ALD models and in humans) are needed to elucidate pathological features and pathogenic mechanisms underlying ALD. Notably, oxidative changes in the liver have been recognized as a signature trait of ALD. Progression of ALD is linked to the generation of highly reactive free radicals by reactions involving ethanol and its metabolites. Furthermore, hepatic oxidative stress promotes tissue injury and, in turn, stimulates inflammatory responses in the liver, forming a pathological loop that promotes the progression of ALD. Accordingly, accumulating further knowledge on the relationship between oxidative stress and inflammation may help establish a viable therapeutic approach for treating ALD.
Highlights
The hepatic manifestation of heavy alcohol consumption is referred to as alcoholic liver disease (ALD), which encompasses a wide spectrum of disorders including fatty liver, alcoholic steatohepatitis (ASH), alcoholic hepatitis (AH), cirrhosis, and hepatocellular carcinoma [6,7,8,9,10]
In the United States, recent studies have reported that approximately 40% of cirrhosisrelated deaths can be attributed to Alcoholic liver disease (ALD), and the three-month mortality of severe AH is approximately 50%, indicating that ALD may be fatal without active therapeutic intervention [16,17]
The involvement of oxidative stress in the pathogenesis of ALD has been previously established, detailed mechanisms underlying the relationship between oxidative stress and diverse pathogenic players of ALD continue to be elucidated, given the expansion in our knowledge regarding cell death, immune reactions, and inflammation in the context of ALD
Summary
Excessive and chronic alcohol intake can cause numerous problems affecting various physiological systems, including the immune, nervous, cardiovascular, and digestive systems [1,2,3,4,5]. The hepatic manifestation of heavy alcohol consumption is referred to as alcoholic liver disease (ALD), which encompasses a wide spectrum of disorders including fatty liver, alcoholic steatohepatitis (ASH), alcoholic hepatitis (AH), cirrhosis, and hepatocellular carcinoma [6,7,8,9,10]. Inflammation, and activation of the liver regeneration machinery, which are features of ASH, may result in the replacement of the hepatic parenchyma with fibrotic tissues, eventually causing liver failure and cirrhosis [12]. Molecular mechanisms underlying the principal features of ALD progression, including liver injury, inflammation, and fibrosis, have been extensively investigated as potential therapeutic targets for ALD [18]. We discuss therapeutic approaches that target oxidative stress and inflammation in ALD
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