TY - JOUR
T1 - Alcoholic liver disease
T2 - a new insight into the pathogenesis of liver disease
AU - Park, Seol Hee
AU - Lee, Young Sun
AU - Sim, Jaemin
AU - Seo, Seonkyung
AU - Seo, Wonhyo
N1 - Funding Information:
This work was supported by the National Research Foundation of Korea (Grant Numbers: 2014M3A9D5A01073556, 2018R1A5A2025286, 2021R1F1A1062136, and 2022R1C1C1008912).
Publisher Copyright:
© 2022, The Pharmaceutical Society of Korea.
PY - 2022/7
Y1 - 2022/7
N2 - Excessive alcohol consumption contributes to a broad clinical spectrum of liver diseases, from simple steatosis to end-stage hepatocellular carcinoma. The liver is the primary organ that metabolizes ingested alcohol and is exquisitely sensitive to alcohol intake. Alcohol metabolism is classified into two pathways: oxidative and non-oxidative alcohol metabolism. Both oxidative and non-oxidative alcohol metabolisms and their metabolites have toxic consequences for multiple organs, including the liver, adipose tissue, intestine, and pancreas. Although many studies have focused on the effects of oxidative alcohol metabolites on liver damage, the importance of non-oxidative alcohol metabolites in cellular damage has also been discovered. Furthermore, extrahepatic alcohol effects are crucial for providing additional information necessary for the progression of alcoholic liver disease. Therefore, studying the effects of alcohol-producing metabolites and interorgan crosstalk between the liver and peripheral organs that express ethanol-metabolizing enzymes will facilitate a comprehensive understanding of the pathogenesis of alcoholic liver disease. This review focuses on alcohol-metabolite-associated hepatotoxicity due to oxidative and non-oxidative alcohol metabolites and the role of interorgan crosstalk in alcoholic liver disease pathogenesis.
AB - Excessive alcohol consumption contributes to a broad clinical spectrum of liver diseases, from simple steatosis to end-stage hepatocellular carcinoma. The liver is the primary organ that metabolizes ingested alcohol and is exquisitely sensitive to alcohol intake. Alcohol metabolism is classified into two pathways: oxidative and non-oxidative alcohol metabolism. Both oxidative and non-oxidative alcohol metabolisms and their metabolites have toxic consequences for multiple organs, including the liver, adipose tissue, intestine, and pancreas. Although many studies have focused on the effects of oxidative alcohol metabolites on liver damage, the importance of non-oxidative alcohol metabolites in cellular damage has also been discovered. Furthermore, extrahepatic alcohol effects are crucial for providing additional information necessary for the progression of alcoholic liver disease. Therefore, studying the effects of alcohol-producing metabolites and interorgan crosstalk between the liver and peripheral organs that express ethanol-metabolizing enzymes will facilitate a comprehensive understanding of the pathogenesis of alcoholic liver disease. This review focuses on alcohol-metabolite-associated hepatotoxicity due to oxidative and non-oxidative alcohol metabolites and the role of interorgan crosstalk in alcoholic liver disease pathogenesis.
KW - Acetaldehyde
KW - Alcoholic liver disease
KW - Fatty acid ethyl esters
KW - Interorgan communication
KW - Non-oxidative alcohol metabolites
KW - Oxidative alcohol metabolites
UR - http://www.scopus.com/inward/record.url?scp=85132903579&partnerID=8YFLogxK
U2 - 10.1007/s12272-022-01392-4
DO - 10.1007/s12272-022-01392-4
M3 - Review article
C2 - 35761115
AN - SCOPUS:85132903579
SN - 0253-6269
VL - 45
SP - 447
EP - 459
JO - Archives of Pharmacal Research
JF - Archives of Pharmacal Research
IS - 7
ER -