Scientists find a new anti-hepatic fibrosis drug target

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Scientists from Russia and Italy studied a new axis of the path that prevents the development of liver fibrosis. The role of the GILZ protein in containing the disease was shown in a study using mouse models and confirmed by clinical data. These results can be used in the treatment of liver fibrosis in humans. The research was published in the journal Cell Death & Disease.

Fibrosis combines connective tissue overgrowth and deterioration in liver function, which can be caused by a viral infection, alcohol poisoning, autoimmune diseases, or other liver diseases. If left untreated, fibrosis can lead to cirrhosis and even death. Inflammatory processes – complex cascades of molecular interactions between the cells of the immune system – play an important role in the progression of fibrosis. Therefore, treating them requires a thorough understanding of these processes at the molecular level. The most common anti-inflammatory agents, such as glucocorticoids, are widely used in the treatment of autoimmune diseases and other problems. However, in liver fibrosis, they can cause serious side effects.

In their most recent study, researchers from Skoltech, the University of Perugia and the University of Florence (Italy) focused on the GILZ protein. GILZ expression leads to changes in cellular processes that are similar to those triggered by glucocorticoids. The team experimented with a model of liver fibrosis induced in GILZ knockout mice and observed rapid disease progression. The scientists tested their hypothesis about the effect of GILZ on the progression of fibrosis using gene expression data in patients with liver fibrosis and obtained evidence of lower GILZ levels in these patients. Down-regulation of the upstream CCR2 protein restored resistance to the progression of liver fibrosis.

The team’s results suggest that GILZ is a promising target for liver fibrosis drugs.

“What is important is that there is a strong correlation between our data on mice and clinical data on humans, which is seldom the case with laboratory results obtained with model objects and even mammals that may never be confirmed in humans. Now we have them all Reason to expect this. ” By controlling the signaling pathway in which GILZ is involved, one could treat inflammatory liver diseases in humans, “explains Professor Timofei Zatsepin from the Skoltech Center for Life Sciences (CLS).

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More information:
Sara Flamini et al. Glucocorticoid-induced leucine zipper regulates liver fibrosis by suppressing CCL2-mediated leukocyte recruitment, cell death, and disease (2021). DOI: 10.1038 / s41419-021-03704-w Provided by the Skolkovo Institute for Science and Technology

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