Scientists identify why alcohol-damaged liver cells stop regenerating

September 5, 2026 at 12:00 AM2 min

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Researchers from the University of Illinois Urbana-Champaign, Duke University, and the Chan Zuckerberg Biohub in Chicago identified the mechanism that blocks liver regeneration in alcohol-related disease. They found that inflammation disrupts RNA splicing and traps liver cells in an immature state, preventing recovery. The findings were published in Nature Communications.

Key Facts

The study was published in Nature Communications by researchers from the University of Illinois Urbana-Champaign, Duke University, and the Chan Zuckerberg Biohub in Chicago.
In patients with alcoholic hepatitis and cirrhosis, liver cells become trapped in an intermediate state between stem-cell-like division and mature function.
Alcohol-induced inflammation sharply reduces levels of the protein ESRP2, which is responsible for correct RNA splicing.
In mouse experiments, blocking inflammatory signals restored normal ESRP2 levels and RNA splicing.

Mechanism of Liver Regeneration Failure

Healthy liver cells respond to damage by temporarily entering a state similar to embryonic stem cells, dividing actively, and then maturing again to perform their functions. Analysis of tissue samples from patients with alcoholic hepatitis and cirrhosis showed that cells become stuck in an intermediate state. These cells lose the ability to work as adult cells but also cannot complete the division process. The resulting increased load on remaining healthy tissue triggers a chain of similar failures and leads to liver failure.

Role of RNA Splicing and ESRP2

The cause of the cell arrest is disruption of RNA splicing, the process of assembling molecular instructions for protein synthesis. Alcohol-induced inflammation sharply reduces the level of the protein ESRP2, which is responsible for correct RNA assembly. As a result, proteins important for regeneration accumulate in the cytoplasm instead of reaching the cell nucleus.

Experimental Findings and Therapeutic Potential

In experiments on mice, blocking inflammatory signals restored normal ESRP2 levels and RNA splicing. The authors expect these findings to help create new diagnostic methods and therapeutic drugs for severe liver damage without the need for organ transplantation.