US EPA

1565859 

Journal Article 

Role of Oxidative Stress and Molecular Changes in Liver Fibrosis: A Review 

Sanchez-Valle, V; Chavez-Tapia, NC; Uribe, M; Mendez-Sanchez, N 

2012 

Yes 

Current Medicinal Chemistry
ISSN: 0929-8673
EISSN: 1875-533X 

19 

28 

4850-4860 

22709007 

WOS:000309745800012 

Liver fibrosis represents a health problem with significant
morbidity and mortality that affects 100 million people worldwide. It is a final pathway to
several chronic liver diseases and is characterized by excess collagen and accumulation of
extracellular matrix in response to chronic hepatocellular damage. Clinical and experimental data
suggest that oxidative stress (OS) mediates the progression of fibrosis, and that OS-related
molecules may act as mediators of molecular and cellular events implicated in liver fibrosis. The
generation of reactive oxygen species (ROS) plays an important role in producing liver damage and
initiating hepatic fibrogenesis. OS disrupts lipids, proteins and DNA, induces necrosis and
apoptosis of hepatocytes and amplifies the inflammatory response. ROS also stimulate the
production of profibrogenic mediators from Kupffer cells and circulating inflammatory cells and
directly activate hepatic stellate cells, resulting in the initiation of fibrosis. Advances in
understanding the mechanisms involved in fibrosis have identified new molecular targets with
therapeutic potential for more targeted and personalized control of this disease. This review
will highlight recent concepts in OS, antioxidants and the molecular pathways involved in hepatic
fibrosis. 

Antioxidants; fibrosis; hepatic stellate cells; liver; oxidative stress; reactive oxygen species; nitric oxide; cytokine; cirrhosis; inflammation