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Liver damage refers to the pathological process whereby hepatocytes and other liver cell types undergo injury and death due to a variety of mechanisms, including oxidative stress, immune-mediated damage, toxic metabolite accumulation, and cellular apoptosis or necrosis[6][5][4]. This process underlies many clinical liver diseases, including acute and chronic hepatitis, fatty liver disease, fibrosis, cirrhosis, and hepatocellular carcinoma[1][2][3]. Liver damage is assessed via biochemical markers (such as aminotransferase levels), histology, and increasingly, molecular and genetic markers to determine severity and guide therapy[2][5][7]. It is not itself a receptor, enzyme, or other discrete molecular target but is the endpoint of many converging pathophysiological pathways.
Drugs may reduce liver damage by anti-inflammatory, anti-oxidant, anti-fibrotic, or cytoprotective effects
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