Heavy alcohol use is the cause of
alcoholic liver disease (ALD). The ALD spectrum ranges from alcoholic steatosis to
steatohepatitis,
fibrosis, and
cirrhosis. In Western countries, approximately 50% of
cirrhosis-related deaths are due to alcohol use. While
alcoholic cirrhosis is no longer considered a completely irreversible condition, no effective anti-fibrotic
therapies are currently available. Another significant clinical aspect of ALD is
alcoholic hepatitis (AH). AH is an acute inflammatory condition that is often comorbid with
cirrhosis, and severe AH has a high mortality rate. Therapeutic options for ALD are limited. The established treatment for AH is
corticosteroids, which improve short-term survival but do not affect long-term survival.
Liver transplantation is a curative treatment option for
alcoholic cirrhosis and AH, but patients must abstain from alcohol use for 6 months to qualify. Additional effective
therapies are needed. The molecular mechanisms underlying ALD are complex and have not been fully elucidated. Various molecules, signaling pathways, and crosstalk between multiple hepatic and extrahepatic cells contribute to ALD progression. This review highlights established and emerging concepts in ALD clinicopathology, their underlying molecular mechanisms, and current and future ALD treatment options.