Krishna Sumanth Nallagangula, Ramesh Pradhan and Shashidhar.K.N*

Liver fibrosis is natural wound healing response to different etiologies of chronic liver insults leading to accumulation of Extra Cellular Matrix (ECM) due to imbalance between synthesis and degradation. Fibrogenesis is consequence of multicellular response; activation of Hepatic Stellate Cells (HSCs) and transdifferentiation into myofibroblasts are crucial for development of hepatic scar. Recent studies evidenced that liver fibrosis is potentially bidirectional regulated by complex cytokines, growth factors, genetic and epigenetic mechanisms (DNA methylation, histone modifications and miRNAs mediated gene silencing). Regression of liver fibrosis is due to increase in collagenolytic activity and increased Metalloproteinase (MMPs) activity with decreased expression and activity of Tissue Inhibitors of Metalloproteinases (TIMPs). Reversible epigenetic mechanisms, pro-fibrotic and anti-fibrotic miRNAs regulate progression and regression of liver fibrosis which initiates to discover diagnostic, prognostic and therapeutic should be comprehensively defined. Hence, in this review we made an attempt to understand molecular, genetic and epigenetic mechanisms of bidirectional liver fibrosis.

Cite this Article: Sumanth NK, Pradhan R, Shashidhar KN. Molecular and Epigenetic Mechanisms of Bidirectional Liver Fibrosis. American J Liver Clinical Res. 2017;1(1):001-006.

Published: 27 December 2017