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The liver changes with age, leading to an impaired ability to respond to hepatic insults and increased incidence of liver disease in the elderly. Therefore, there is critical need for rapid model systems to study aging‐related liver changes. One potential opportunity is murine models of human progerias or diseases of accelerated aging. Ercc1^−/Δ mice model a rare human progeroid syndrome caused by inherited defects in DNA repair. To determine whether hepatic changes that occur with normal aging occur prematurely in Ercc1^−/Δ mice, we systematically compared liver from 5‐month‐old progeroid Ercc1^−/Δ mice to old (24‐36‐month‐old) wild‐type (WT) mice. Both displayed areas of necrosis, foci of hepatocellular degeneration, and acute inflammation. Loss of hepatic architecture, fibrosis, steatosis, pseudocapillarization, and anisokaryosis were more dramatic in Ercc1^−/Δ mice than in old WT mice. Liver enzymes …