Researchers have uncovered a new pathway that helps explain how consuming too much alcohol causes damage to the liver, specifically mitochondrial dysfunction in alcohol-associated liver disease.

The discovery, published in the peer-reviewed journal Nature Communications, can also help lead to a new treatment approach for people suffering from the disease.

Cases of alcohol-associated liver disease continue to rise and is one of the leading causes of alcohol-related deaths. The spectrum of the disease includes hepatitis, fibrosis to cirrhosis and liver cancer. Cirrhosis alone causes 1.6 million deaths worldwide and over 50% of cases are due to alcohol abuse. Besides abstinence, there currently are no effective therapies for treating people with the disease.

«Alcohol-associated liver disease is a major problem in the world,» said Shelly C. Lu, MD, director of the Karsh Division of Gastroenterology and Hepatology in the Department of Medicine and senior author of the study. «We’ve known for a long time that alcohol somehow damages mitochondria, but until now, it’s not been clear as to what the mechanisms are for this damage to occur.»

The liver is very rich in mitochondria, known as the powerhouse of all cells, and plays a critical role in liver function. Alcohol, however, can alter the structure and function of the mitochondria, leading to liver injury.

To better understand the mechanisms for mitochondrial damage in alcohol-associated liver disease, Lu and her team looked at the role of an enzyme called MAT?1 that’s responsible for providing the liver vital nutrients for survival.

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Materials provided by Cedars-Sinai Medical Center. Note: Content may be edited for style and length.