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Activity-based sensing reveals elevated labile copper promotes liver aging via hepatic ALDH1A1 depletion
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Activity-based sensing reveals elevated labile copper promotes liver aging via hepatic ALDH1A1 depletion
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Journal Article
Activity-based sensing reveals elevated labile copper promotes liver aging via hepatic ALDH1A1 depletion
2025
Overview
Oxidative stress plays a key role in aging and related diseases, including neurodegeneration, cancer, and organ failure. Copper (Cu), a redox-active metal ion, generates reactive oxygen species (ROS), and its dysregulation contributes to aging. Here, we develop activity-based imaging probes for the sensitive detection of Cu(I) and show that labile hepatic Cu activity increases with age, paralleling a decline in ALDH1A1 activity, a protective hepatic enzyme. We also observe an age-related decrease in hepatic glutathione (GSH) activity through noninvasive photoacoustic imaging. Using these probes, we perform longitudinal studies in aged mice treated with ATN-224, a Cu chelator, and demonstrate that this treatment improves Cu homeostasis and preserves ALDH1A1 activity. Our findings uncover a direct link between Cu dysregulation and aging, providing insights into its role and offering a therapeutic strategy to mitigate its effects.
Copper (Cu) dysregulation contributes to aging and oxidative stress. Here the authors develop imaging probes to detect labile hepatic Cu, revealing age-related increases that deplete ALDH1A1 activity, and show that chelation therapy restores Cu homeostasis, offering a potential strategy to mitigate liver aging.
Publisher
Nature Publishing Group UK,Nature Publishing Group,Nature Portfolio
