EFHD1 may turn fatty liver disease into injury, with inhibition reducing scarring by up to 60%

University of Utah researchers have discovered that the protein EFHD1 drives the progression of fatty liver disease into severe injury. Blocking this protein in laboratory models reduced liver scarring by up to 60%, offering a potential pathway for new drug therapies.
Why it matters
Metabolic liver disease is a growing global health concern, and this research offers a new mechanism to prevent irreversible organ damage.
edited by Swati Mestri , reviewed by Robert Egan
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Add as preferred source Fluorescent microscope image of a healthy liver cell. Mitochondria (green) are compact and bean-shaped. Credit: Dipayan Chaudhuri Obesity-related metabolic liver disease affects hundreds of millions of people worldwide, but only some of those livers develop scarring, become inflamed and eventually fail. University of Utah researchers have identified a protein, EFHD1, that appears to drive that transition by triggering an out-of-place antiviral immune response.
They also demonstrated that blocking the protein can protect against liver injury in human cells and mouse models, even on a high-fat diet—paving the way for therapies to prevent liver damage.
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