Researchers identify mechanism blocking liver regeneration after alcohol consumption

Researchers from the University of Illinois Urbana-Champaign, Duke University, and the Chan Zuckerberg Biohub Chicago have identified why the liver fails to regenerate in patients with alcoholic hepatitis and cirrhosis, even after they cease alcohol consumption.

According to the study published in Nature Communications, alcohol-induced inflammation suppresses the ESRP2 protein. This suppression disrupts RNA splicing, a vital cellular process that converts genetic instructions into functional proteins. Consequently, liver cells become trapped in an unproductive, intermediate state—neither fully functional adult cells nor active progenitor cells capable of division.

This cellular limbo creates a cycle where the inability of cells to regenerate places increased pressure on remaining functional cells, which then also risk becoming trapped in this non-functional state. Alcohol-related liver disease is a leading cause of global liver mortality, linked to approximately 3 million deaths annually. Scientists noted that understanding this mechanism could eventually lead to interventions beyond liver transplantation.