A study published in Nature Metabolism identifies the enzyme UBE2N as a potential target for preventing the progression of metabolic dysfunction-associated steatotic liver disease.
Key facts
- •Approximately 100 million people in the U.S. are estimated to have metabolic dysfunction-associated steatotic liver disease.
- •MASH is a severe form of liver disease that involves inflammation, cell injury, and scarring.
- •Researchers found that UBE2N levels decrease as liver disease progresses, leading to more damaged cells.
- •Restoring UBE2N in laboratory mice reduced fat accumulation, inflammation, and scarring in the liver.
- •The study was published in the journal Nature Metabolism and involved a multicenter research team.
Researchers co-led by Cedars-Sinai Health Sciences University have identified an enzyme, UBE2N, that may protect the liver from damage associated with the progression of metabolic dysfunction-associated steatotic liver disease (MASLD). The preclinical study, published in Nature Metabolism, suggests that restoring levels of this enzyme could help prevent the condition from advancing to the more severe metabolic dysfunction-associated steatohepatitis (MASH).
By the numbers
Role of UBE2N in Liver Health
In the study, researchers observed that levels of the UBE2N enzyme decline in liver cells as MASLD becomes more advanced. According to Ekihiro Seki, a co-corresponding author of the study, the enzyme helps protect the liver by facilitating the removal of damaged mitochondria—the energy-producing structures in cells—and supporting the breakdown of fat. When researchers restored UBE2N to normal levels in laboratory mice, they observed a reduction in liver inflammation, scarring, and fat accumulation.
Context and Future Research
MASLD affects an estimated 100 million people in the United States, with 20% to 25% of those individuals developing MASH, a condition characterized by inflammation, cell injury, and scarring. Currently, there is no cure for MASH, and treatment options are limited to lifestyle changes and efforts to mitigate further liver damage. Shelly Lu, director of the Karsh Division of Gastroenterology and Hepatology at Cedars-Sinai, noted that future studies will be needed to determine if enhancing this protective pathway can complement existing treatments and lead to new therapeutic approaches.
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This article was independently rewritten by ManyPress editorial AI from reporting originally published by ScienceDaily.
