This sparks hope for human treatment.
Liver fibrosis, a serious stiffening of liver tissue often caused by cirrhosis or hepatitis infections, is typically irreversible and can be life-threatening. For many patients with severe liver damage, a transplant is their only hope. However, new research from Cedars-Sinai in Los Angeles has raised the possibility of reversing liver fibrosis in a groundbreaking study involving mice.
According to recent findings published in Nature Communications, Cedars-Sinai researchers have identified a genetic pathway that could potentially stop fibrosis in its tracks. The research team, led by Dr. Shelly Lu, discovered three key genes — FOXM1, MAT2A, and MAT2B — that play critical roles in the progression of liver fibrosis. Dr. Lu, head of the gastroenterology and hepatology department, highlighted the potential of these genes as targets for new drug treatments. Blocking proteins produced by any of these genes could offer a new approach to treat liver fibrosis.
The study is in its early stages, and results in animal models do not always translate directly to human applications. However, Dr. Peter Chen, chair of the Department of Medicine at Cedars-Sinai, emphasized the importance of these findings for expanding treatment options. While not involved in the research, Dr. Chen called the study a significant step forward in understanding and potentially addressing liver fibrosis.
The researchers zeroed in on the three genes involved in fibrosis. FOXM1, active in liver cells known as hepatocytes, can drive cancer, inflammation, and fibrosis when overactive. MAT2A and MAT2B are active in stellate cells, another cell type involved in fibrotic development. Together, these genes produce proteins that communicate with one another within liver cells, fueling inflammation and fibrosis. The researchers also noted that these proteins use extracellular vesicles to send genetic information to nearby cells, amplifying the fibrotic process.
To test whether inhibiting one of these proteins could halt fibrosis, Dr. Lu’s team first induced fibrosis in mice. They then treated the mice with FDI-6, a substance that blocks the protein from the FOXM1 gene. The treatment not only stopped further fibrosis but also seemed to reverse some of the existing scarring in liver tissue.
While this study offers an encouraging breakthrough, further research is needed to determine if similar treatments could benefit humans. Since the genes involved are shared by both mice and humans, the findings provide a hopeful foundation for future therapeutic approaches to liver fibrosis.
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