The Duke University team conducted experiments using mouse and human liver tissue to determine how the aging process promotes the death of certain liver cells in these tissues. Subsequently, they successfully reversed the aging process of the liver using drugs. This research result is expected to benefit millions of liver injury patients. The relevant paper was published in the latest issue of the journal Nature Aging. This time, the team discovered a unique genetic feature of the aging liver. Compared to young livers, aging livers have a large number of genes activated, leading to degeneration of the liver's main functional cells - hepatocytes. Due to aging, it promotes a programmed cell death in liver cells that relies on iron, a process known as ferroptosis. Metabolic stressors can amplify this death process and increase liver damage. The team utilized this genetic feature to analyze human liver tissue and found that the livers of obese and non-alcoholic liver disease patients also exhibit this feature. Moreover, the more severe the disease, the more obvious this characteristic becomes. Importantly, key genes in the liver of these patients are highly activated, promoting cell death through iron deficiency anemia. This provides a clear target. The team then fed specific foods to young and old mice, causing them to develop non-alcoholic liver disease. Then, they gave half of the animals a placebo; The other half takes the drug Ferrostatin-1, which can inhibit the pathway of cell death. The results indicate that the liver of mice taking Ferrostatin-1 is biologically similar to that of young and healthy livers. This study shows that aging can lead to ferritin stress, exacerbating non-alcoholic liver disease. By reducing the impact of this stress, liver damage can be reversed. (Lai Xin She)