Topic: Genetic and Epigenetic Factors in Liver Disease Pathogenesis

Genetic disorders, alcohol abuse, drugs, cholestasis, chronic viral hepatitis, parasitic infections and various cryptogenic causes are the major factors that provoke liver disease. In addition, the prevalence of metabolic dysfunction-associated fatty liver disease (MAFLD) is increasing worldwide. Regardless of the underlying cause, liver injury is associated with inflammation and progressive extracellular matrix accumulation. If left untreated, liver disease leads to a disruption of the lobular structure of the liver and a progressive decline in hepatocellular function. While research over the past few decades has identified numerous soluble mediators, molecular pathways, and profibrogenic genes that play a key role in the development of liver disease, effective therapies to combat these diseases are limited. However, independent experimental studies and clinical trials have identified several potential soluble and cellular drug targets that are critically involved in the inflammatory process and extracellular matrix production. This knowledge offers hope for the development of new therapies to address the pathogenesis of liver disease.

In this Special Issue of Journal of Translational Genetics and Genomics (JTGG), I invite you to submit original research articles, reviews, or shorter perspective articles on all aspects related to the topic “Genetic and Epigenetic Factors in Liver Disease Pathogenesis”. In particular, articles describing novel mechanistic insights into the impact of genetic or epigenetic factors on liver disease are highly encouraged. Relevant topics include but are not limited to:

● Monogenic diseases causing parenchymal damage;

● Monogenic diseases with both hepatic and extrahepatic manifestations;

● Genetic variants and polygenic traits in liver disease;

● Genetic testing in the clinical management of liver disease;

● DNA methylation in the pathogenesis of liver disease;

● Histone modifications and chromatin remodeling in liver disease;

● Epigenetic and genetic modifiers of metabolic dysfunction-associated steatohepatitis (MASH);

● The impact of non-coding RNA on liver disease outcomes;

● Oncogenic roles of viruses in the pathogenesis of liver disease;

● Epigenetic imprinting in human liver disease;

● Emerging epigenetic therapies for liver disease.

I look forward to your contributions to this important area of research.

Ralf Weiskirchen