Abstract
Chronic alcohol consumption is a major cause of death worldwide. Chronic, heavy alcohol consumption leads to alcoholic liver disease (ALD), which progresses from steatosis to steatohepatitis, with the eventual development of fibrosis and cirrhosis in many heavy drinkers. Recent evidence indicates that multiple stages of ALD, including fibrosis, are reversible, thus understanding the underlying molecular mechanisms involved in the progression of ALD is critical. Hepatic stellate cells (HSCs) play a major role in the progression of ALD to fibrosis. Metabolism of alcohol in the liver results in the activation and proliferation of HSCs mediated, at least in part, by factors released from both hepatocytes and Kupffer cells, the resident liver macrophages. Here we review our current understanding of the specific pathways by which alcohol and alcohol metabolism contribute to the activation of HSC and the progression of fibrosis.
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