2023
DOI: 10.1111/jgh.16282
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Alcohol and the mechanisms of liver disease

Abstract: Alcoholic liver disease (ALD), which is a leading cause of morbidity and mortality worldwide, covers a large spectrum of liver injuries ranging from simple steatosis to steatohepatitis, advanced fibrosis, cirrhosis, and hepatocellular carcinoma. The pathogenesis of ALD includes genetic and epigenetic alterations, oxidative stress, acetaldehyde-mediated toxicity and cytokine and chemokine-induced inflammation, metabolic reprogramming, immune damage, and dysbiosis of the gut microbiota. This review discusses the… Show more

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Cited by 16 publications
(5 citation statements)
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“…Accumulating evidence suggested that hepatic oxidative stress and inflammatory responses play a central and causal role in the pathological process of ALD [ 25 , 26 ]. Malondialdehyde (MDA), a lipid peroxidation product, can unspecifically bind with proteins to form adducts, resulting in dysfunction of protein and cellular homeostasis disorders [ 27 , 28 ]. Our data showed that PGF significantly inhibited MDA levels in the alcoholic liver.…”
Section: Discussionmentioning
confidence: 99%
“…Accumulating evidence suggested that hepatic oxidative stress and inflammatory responses play a central and causal role in the pathological process of ALD [ 25 , 26 ]. Malondialdehyde (MDA), a lipid peroxidation product, can unspecifically bind with proteins to form adducts, resulting in dysfunction of protein and cellular homeostasis disorders [ 27 , 28 ]. Our data showed that PGF significantly inhibited MDA levels in the alcoholic liver.…”
Section: Discussionmentioning
confidence: 99%
“…Ethanol triggers unrestrained inflammation and immune turbulence via regulating key cell subsets in the hepatic immune microenvironment. Kupffer cells (KC) (liver-resident macrophages) play a crucial role in the innate immune response against infections and initiating and resolving inflammation ( Yao et al, 2017 ; Chen M. et al, 2023 ). Chronic alcohol consumption impairs the intestinal mucosal barrier, leading to increase permeability and translocation of intestinal Gram-negative bacteria-derived lipopolysaccharide (LPS) to the liver.…”
Section: Pathophysiology Of Aldmentioning
confidence: 99%
“…ALD development and progression often involve gene activation and suppression without changes in DNA sequence [4][5][6][7][8][9][10]. These changes are mediated by histone and DNA modifications that are part of the spectrum of epigenetic modifications.…”
Section: Epigenetics In Ald Progressionmentioning
confidence: 99%