Nuclear Factor Erythroid 2-Related Factor 2 Versus Reactive Oxygen Species: Potential Therapeutic Approach on Fighting Liver Fibrosis

Chronic liver disease (CLD) is a progressive deterioration of the due to exposure viruses, drugs, fat accumulation, and toxicity which lead an imbalance between extracellular matrix accumulation degradation. Accumulation normal response at beginning injury. However, increasing leads fibrosis, cirrhosis, organ failure. Until today, transplant gold standard therapy for end-stage CLD. Unfortunately, itself faces difficulties such as finding compatible donor dealing with complications after treatment. This review provides further information about nuclear factor erythroid 2-related 2 (Nrf2) alternative approach fight fibrosis. Transformation hepatic stellate cell (HSC) myofibroblast has been known main mechanism that occurs in fibrosis while epithelial-mesenchymal transition (EMT) mitochondrial dysfunction become followed. In these conditions, oxidative stress great promoter builds vicious cycle leading CLD progressivity. Hence, Nrf2 antioxidant regulator becomes potential target break cycle. While reactive oxygen species (ROS) induce HSC activation, EMT, through activation many signaling pathways, acts diminish ROS directly by regulating secreted antioxidants its scavenging action. also inactivates pathways plays role maintaining health. Therefore, can be therapy.