Researchers from the Kalsotra and Diehl labs have discovered why alcohol-associated liver disease impairs regeneration. Normally, liver cells temporarily revert to a fetal, like state to multiply and then mature. But in diseased livers, cells get trapped in a dysfunctional “quasi-progenitor” state, unable to regenerate or function properly.
The root cause is widespread RNA missplicing, genetic instructions are stitched incorrectly, leading to mislocalized proteins. A key splicing regulator, ESRP2, is missing in damaged livers due to inflammatory signals from immune and support cells.
