Abstract
Abstract Autoimmune liver disease, including autoimmune hepatitis, primary biliary cholangitis, and primary sclerosing cholangitis, is a chronic autoimmune liver condition characterized by abnormal accumulation of proinflammatory immune cells. As more and more genetic studies are conducted, it is becoming increasingly clear that genetic risk cannot fully explain disease pathogenesis. Epigenetic modifications, including CpG island DNA methylation, histone modification, and microRNA-mediated gene silencing, are gradually being acknowledged to play a role in immune cellular identity and disease heterogeneity. Given the heterogeneity and environmental exposure bias observed in patients, it is essential to uncover the epigenetic mechanisms of autoimmune liver disease, which could integrate environmental skewing, cell lineage commitment, and genetics to provide a fuller mechanistic understanding of the disease. Epigenetic profiling holds promise for identifying diagnostic and prognostic biomarkers, and epigenetic manipulations could result in novel therapies. Cutting-edge breakthroughs are frequently being made in epigenetics, which might guide future explorations into autoimmune liver disease.
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