Semin Liver Dis 2017; 37(03): 219-230
DOI: 10.1055/s-0037-1605371
Review Article
Thieme Medical Publishers 333 Seventh Avenue, New York, NY 10001, USA.

Epigenetics in Liver Fibrosis

Veronica Massey1, Joaquin Cabezas2, 3, Ramon Bataller1, 4, 5
  • 1Bowles Center for Alcohol Studies, University of North Carolina at Chapel Hill, School of Medicine, Chapel Hill, North Carolina
  • 2 Department of Gastroenterology and Hepatology, University Hospital Marques de Valdecilla, Santander, Spain
  • 3Valdecilla Research Institute – IDIVAL, Santander, Spain
  • 4Division of Gastroenterology and Hepatology, Departments of Medicine and Nutrition, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina
  • 5Division of Gastroenterology, Hepatology and Nutrition, University of Pittsburgh Medical Center, Pennsylvania
Further Information

Publication History

Publication Date:
28 August 2017 (online)


Liver fibrosis is a common consequence of chronic liver injury and is a key determinant of liver-associated morbidity and mortality. Identification of new mechanisms of fibrosis, including disease-specific molecular drivers, remains relevant to reveal novel biomarkers and therapeutic targets. Recently, greater accessibility to more advanced molecular methods that can assess changes in epigenetic regulation has stimulated more research investigating the epigenetic landscape of liver fibrosis. Such studies have revealed changes in DNA methylation, histone acetylation, and microRNAs that regulate the fibrogenic response to injury including hepatic stellate cell activation. The aim of this review is to briefly introduce the general mechanisms and epigenetic regulation of liver fibrosis and to familiarize the reader with the chief epigenetic mechanisms implicated as drivers of liver fibrosis.