Scientists from Russia and Italy studied a new axis of the pathway that prevents the development of liver fibrosis. The part of GILZ protein in controlling the disease progression was revealed in a study with mice models and supported by clinical information. These findings may be utilised in treating liver fibrosis in humans. The study was published in the journal Cell Death & Disease.
Fibrosis combines an overgrowth of connective tissue along with a decrease in the liver function Which Can Be Brought on by a viral infection, alcohol intoxication, autoimmune disorders or other liver disorders. If left untreated, fibrosis can lead to cirrhosis and even death. Inflammatory processes–complicated cascades of molecular connections between the cells of the immune system–play a significant role in the progression of fibrosis, consequently, its therapy demands thorough understanding of these processes at the molecular level. The most common anti-inflammatory brokers, like glucocorticoids, are widely utilized in treating autoimmune diseases and other difficulties, however, in the case of liver fibrosis, they will likely cause severe side effects.
In their latest study, researchers in Skoltech, the University of Perugia, and the University of Florence (Italy) centered to the GILZ protein. GILZ expression contributes to changes in cellular processes very similar to those triggered by glucocorticoids. The group experimented with a version of liver fibrosis induced in GILZ knockout mice and detected rapid progression of the illness. The scientists confirmed their hypothesis about the effect of GILZ about the development of fibrosis using gene expression data on patients with liver fibrosis and got evidence of reduced GILZ amounts in these patients. Downregulation of the upstream CCR2 protein restored immunity to the progression of liver fibrosis.
The group’s findings imply that GILZ is a promising anti-hepatic fibrosis drug goal.
“Importantly, there is a strong correlation between our data on mice and clinical data on humans, which is rarely the case with lab results obtained using model objects and even mammals that may never be confirmed in humans. Now we have every reason to expect that by controlling the signaling pathway which involves GILZ, one could treat inflammatory liver diseases in humans,” professor Timofei Zatsepin of their Skoltech Center for Life Sciences (CLS) explains.
Sara Flamini et al.. Glucocorticoid-induced leucine zipper regulates liver fibrosis by suppressing CCL2-mediated leukocyte recruitment, Cell Death & Disease (2021). DOI: 10. 1038/s41419-021-03704-w
Scientists locate a new anti-hepatic fibrosis drug goal (2021, May 4)
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