Restoring enzyme involved in cellular cleanup could reduce inflammation and scarring from liver disease MASH
A team of investigators co-led by Cedars-Sinai Health Sciences University has identified an enzyme that helps prevent the most common form of liver disease from progressing toward liver failure. Results of the preclinical study, published in Nature Metabolism, could point the way to new approaches for preventing serious organ damage.
A team of researchers led by Cedars-Sinai Health Sciences University has discovered an enzyme called UBE2N that plays a crucial role in preventing the progression of the most common form of liver disease, metabolic dysfunction-associated steatotic liver disease (MASLD), towards liver failure. The study, published in Nature Metabolism, could pave the way for new treatments to prevent serious organ damage.
MASLD, previously known as nonalcoholic fatty liver disease, affects an estimated 100 million people in the United States, with around 20% to 25% of cases progressing to a more severe form called metabolic dysfunction-associated steatohepatitis (MASH). In MASH, excess fat accumulation in the liver leads to inflammation, cell damage, and scarring, with no cure currently available. Existing treatments mainly involve lifestyle changes and protecting the liver from further damage, with limited effective medications available.
Previous research suggested that damaged mitochondria, which provide energy to cells, were a key driver of MASH. However, the new multicenter study by Cedars-Sinai investigators identified that the UBE2N enzyme levels decrease in liver cells as the disease progresses. It appears that UBE2N helps protect the liver by removing damaged mitochondria and supporting the breakdown of fat.
When the enzyme's levels fell, there was increased cell damage and liver injury. Restoring UBE2N to normal levels in laboratory mice reduced fat buildup, scarring, and inflammation in the liver.
Lead researcher Ekihiro Seki, MD, PhD, stated that the enzyme plays a protective role in the liver by aiding in the removal of damaged mitochondria and promoting fat breakdown. The findings support the UBE2N enzyme as a promising target for preventing MASLD from advancing to MASH.
Cedars-Sinai's Shelly Lu, MD, highlighted the importance of understanding the enzyme's role in regulating mitochondria in the liver for advancing steatotic liver disease. Future studies can explore whether enhancing this protective pathway can complement existing treatments, identify patients most likely to benefit, and lead to new therapeutic approaches for preventing advanced liver disease.
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