Cedars-Sinai researchers identify UBE2N enzyme role in protecting against liver damage

A multicenter study co-led by Cedars-Sinai Health Sciences University found that the enzyme UBE2N protects liver cells by removing damaged mitochondria and aiding fat breakdown.

Researchers discovered that levels of the UBE2N enzyme decline in liver cells as fatty liver disease advances. According to the study published in Nature Metabolism, restoring UBE2N to normal levels in laboratory mice resulted in reductions in fat accumulation, inflammation, and scarring. These findings suggest the enzyme could serve as a potential treatment target for preventing the progression of liver injury.

Ekihiro Seki, MD, PhD, a professor at Cedars-Sinai and co-corresponding author, stated that UBE2N appears to protect the liver from inflammation and damage associated with metabolic dysfunction-associated steatohepatitis (MASH). Dr. Seki noted that when enzyme levels fell in the study, researchers observed more damaged cells and injury to the liver.

Shelly Lu, MD, director of the Karsh Division of Gastroenterology and Hepatology at Cedars-Sinai, described the identification of the enzyme's role as an important advance in understanding steatotic liver disease. Future research may test whether enhancing this pathway can complement existing treatments, which currently center on lifestyle changes as there is no cure for MASH.

Background

According to the American Liver Foundation, an estimated 100 million people in the U.S. have metabolic dysfunction-associated steatotic liver disease (MASLD). Roughly 20% to 25% of those affected develop MASH, a more serious form involving excess liver fat, inflammation, and cell injury.