Targeting TAZ can essentially stop fibrosis and may provide future treatment options for patients with nonalcoholic steatohepatitis.
Targeting TAZ in liver cells and rendering it inactive was found to stop fibrosis in mice with nonalcoholic steatohepatitis (NASH).
The incidence of nonalcoholic fatty liver disease (NAFLD) is continuing to increase, and although it can generally be benign, 1 in 5 individuals with NAFLD will have their disease evolve into NASH.
NASH is a serious condition where the liver becomes inflamed, fibrous scar tissue forms, and liver cells begin to die off. Furthermore, individuals with NASH have an increased risk of liver failure or liver cancer. Unfortunately, there are no current treatment options available for this disease.
Since the amount of fibrosis in the liver has been associated with a greater risk of death from NASH, researchers wanted to find a way to stop fibrosis in a NASH mouse model.
The results of a study published in Cell Metabolism showed that TAZ played a critical role in initiating fibrosis. When TAZ was inactivated, researchers found that the fibrosis had stopped in mice.
Furthermore, the existing fibers in the liver dissolved and essentially the disease disappeared, according to the study.
Additional findings showed a reduction in inflammation and cell death as a result of TAZ being shut off. There was no effect on fat accumulation in the liver. Researchers hypothesize that TAZ works the same way in people as it does in the mice.
“We think that by stopping fibrosis through TAZ and its partners, we may be able to prevent the serious consequences of NASH, including liver failure and liver cancer,” said researcher Ira Tabas.