Scientists have successfully cured liver fibrosis in mice and brought hope to humans

As a result of cirrhosis, hepatitis and other causes, liver fibrosis can develop – a potentially life-threatening thickening of the tissue, upon onset of which the process becomes irreversible. For many patients, the only hope is a liver transplant. However, a study conducted at Cedars-Sinai Hospital in Los Angeles may give patients hope. Scientists say they have been able to successfully reverse liver fibrosis in mice.

As reported in the journal Nature Communications, scientists have discovered a genetic pathway, blocking which can lead to a complete cessation of fibrosis.

The three genes involved in the process of fibrosis development are called FOXM1, MAT2A and MAT2B.

“We have succeeded in uncovering the FOXM1, MAT2A and MAT2B axis as a potential target for drug development to treat liver fibrosis,” said senior study author Dr. Shelly Lu, chief of the Division of Gastroenterology and Hepatology at Cedars-Sinai. – “Our results suggest that blocking any of these [gene-produced] proteins may be of help in treating this disease.”

Of course, the research is still in its early stages, and results obtained in animals are not always confirmed in humans.

This very promising study significantly deepens our understanding of an insidious disease that too often leaves patients and doctors with very few treatment options.

The research team focused on three genes.

One of them, FOXM1, is present in liver cells called hepatocytes and, when overactive, can cause liver cancer, inflammation and fibrosis.

The other two genes, MAT2A and MAT2B, are active in a second type of liver cells called stellate cells, which also play a role in fibrosis.

All three genes encode different proteins necessary for the development of fibrosis, the scientists explained.

The scientists found that these proteins “talk” to each other inside liver cells. They even influence neighboring cells through extracellular vesicles – fatty molecules filled with genetic fragments, proteins and other biological materials that act as messengers between cells.

Acting together, these proteins stimulate each other, causing inflammation and fibrosis in the liver.

What if the production of even one of the proteins produced by the genetic trio is interrupted?

To find out, Lu’s group first induced liver inflammation and fibrosis in laboratory mice. The mice were then treated with a substance known as FDI-6, which blocks a protein produced by the FOXM1 gene.

The result was impressive: not only did the therapy halt the further development of fibrosis, but it also seemed to reverse some of the fibrotic scarring that had already occurred in the mouse liver tissue.

This is an encouraging start, and the team noted that mice and humans have all three of the genes this study focused on. However, Lu and colleagues emphasized that only further research can determine whether drugs like FDI-6 will help humans.