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Taken together, these results suggest that CPP-CAND inhibited the FOXO4-p53 interaction in the nucleus, which enabled the extranuclear transport of p53 and selectively induced apoptosis in senescent cells

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Using this mechanistic model of bile acids, we explain how abnormal bile acid physiology drives disease pathogenesis, emphasizing how ceramide synthesis may serve as a unifying pathogenic feature for cardiometabolic diseases

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