Inhibition of NOX4 enzyme plays an important role in liver fibrosis

Published on November 5, 2012 at 11:33 PM · No Comments

Researchers at the Bellvitge Biomedical Research Institute (IDIBELL) have led a study published in PLoS One showing that the inhibition of a family member of NADPH oxidase enzyme, NOX4, plays an important role in liver fibrosis.

The researchers studied the function of a cytokine called transforming growth factor-beta (TGF-beta) in the pathophysiology of the liver, which is one of the main research lines of the Biological Clues of the Invasive and Metastatic Phenotype research group at the IDIBELL, leaded by Isabel Fabregat.

This paper is related with the processes of liver fibrosis, an illness caused by the overproduction of extracellular matrix proteins in the liver tissue. During fibrosis, levels of TGF-beta are increased, and there is an activation of the extracellular matrix producing the activation of protecting cells of the extracellular matrix and other possible events leading to the death of hepatocytes.

Two sides

The TGF-beta is a complex cytokine. It is a prominent tumor suppressor in early stages of tumor formation, but, in advanced stages, the cells adapt to escape from the growth inhibitory signals and, under these conditions, the TGF-beta is able to potentiate tumor progression contributing to metastasis.

The study published in PLoS One is a collaboration between IDIBELL and the research group of Wolfgang Mikulits, coauthor of the study, at the Cancer Research Institute of the Medical University of Vienna (Austria), that have provided cellular and animal models. The analysis in patient samples has been possible thanks to the collaboration with the University Hospital Alcorcon Foundation and the Complutense University of Madrid.

The aim of the study was to analyze routes below TGF-beta, i.e. the cytokine-induced pathways that may be responsible for the process leading to the occurrence of fibrosis, cell activation and production of extracellular matrix and the hepatocytes death.

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