Key regulators of hepatic stellate cell activation in alcohol liver Disease: A comprehensive review

•Alcoholic liver disease (ALD) is a wide-ranging group of conditions that start with damage to the liver, progress to liver fibrosis, and ultimately culminate in alcohol-induced liver cirrhosis, which is the most severe and irreversible form of liver damage.•Liver fibrosis (LF) is a frequent pathological feature observed in most chronic liver inflammatory disorders that involve sustained inflammation.•We have summarized ethanol-mediated hepatic stellate cell (HSCs) activation and its role in liver fibrosis progression.•We emphasize the important molecular mechanisms that are influenced by ethanol, participate in the activation of hepatic stellate cells (HSCs), and contribute to the progression of liver fibrosis. Additionally, we identify potential targets that could be utilized to alleviate liver fibrosis. Alcoholic liver disease (ALD) is a broad category of disorders that begin with liver injury, lead to liver fibrosis, and ultimately conclude in alcohol-induced liver cirrhosis, the most chronic and irreversible liver damage. Liver fibrosis (LF) is a common pathological characteristic observed in most chronic liver inflammatory conditions that involve prolonged inflammation. In this review, we have summarized ethanol-mediated hepatic stellate cell (HSCs) activation and its role in liver fibrosis progression. We highlight important molecular mechanisms that are modulated by ethanol, play a role in the activation of HSCs and the progression of liver fibrosis and identifying potential targets to ameliorate liver fibrosis.