Scientists have successfully cured liver fibrosis in mice, offering hope for future treatments in humans.

For many patients, a liver transplant is the only hope. However, a study conducted at Cedars-Sinai Medical Center in Los Angeles may provide patients with optimism. Researchers claim they have successfully reversed liver fibrosis in mice.

As reported in the journal Nature Communications, scientists discovered a genetic pathway whose blockage could lead to the complete cessation of fibrosis.

Three genes involved in the development of fibrosis are named FOXM1, MAT2A, and MAT2B.

“We have revealed the FOXM1, MAT2A, and MAT2B axis as a potential target for drug development to treat liver fibrosis,” says the study's senior author, Dr. Shelly Lu, head of the Division of Gastroenterology and Hepatology at Cedars-Sinai. “Our findings suggest that inhibiting any of these [‘gene-derived’] proteins could aid in treating this disease.”

Of course, the research is still in its early stages, and results obtained in animals do not always translate to humans.

This promising research significantly deepens our understanding of a treacherous disease that often leaves patients and doctors with virtually no treatment options.

The research team focused on three genes.

One of them, FOXM1, is present in liver cells called hepatocytes and, when overly active, can lead to liver cancer, inflammation, and fibrosis.

The other two genes, MAT2A and MAT2B, are active in a second type of liver cells known as 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 researchers found that these proteins “communicate” with each other within 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.

Working together, these proteins stimulate each other, causing inflammation and liver fibrosis.

But what if the production of at least one of the proteins produced by this genetic trio is interrupted?

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

The result was impressive: the therapy not only halted further development of fibrosis but also appeared to reverse some of the already existing fibrous scars in the liver tissue of the mice.

This is a hopeful start, and the team noted that both mice and humans possess all three genes focused on in this study. Nonetheless, Lu and his colleagues emphasized that only further research can determine whether drugs like FDI-6 will be beneficial for humans.