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Liver fibrosis: Open the windows!



Following the publication of our work in Hepatology we propose BMP9 as a new therapeutic target for the treatment of hepatic fibrosis
Published on 24 June 2019
When liver cells are aggressed by viruses or chemicals, they produce scar-like tissue. Its pathological accumulation is called fibrosis.

The BMP family in angiogenesis and lymphangiogenesis team (BAL) at our laboratory has identified a key protein in this process: BMP9. Mice whose BMP9 gene has been inactivated spontaneously develop hepatic fibrosis. Normally, the endothelial cells that form the blood capillaries of the liver have many pores (fenestrae) that ensure exchanges between the blood and liver cells. By looking more closely at these cells under a scanning electron microscope, the researchers found that, in mice lacking the BMP9 gene, the hepatic blood capillaries have lost their fenestrae (picture). In addition, addition of BMP9 prevents this loss of fenestrae, indicating that the protein is essential for the liver to function properly.

BMP9 is thus now considered as a new therapeutic target for the treatment of hepatic fibrosis.

 
The capillary endothelial cells of a normal liver (left) have pores, called fenestrae, visible under a scanning electron microscope. In mice where BMP9 is inactivated (right), the absence of these fenestrae in these cells leads to liver fibrosis.

Credit: Agnès Desroches-Castan and Emmanuelle Tillet, Inserm U1036

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