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- W4313594705 endingPage "141313" @default.
- W4313594705 startingPage "141313" @default.
- W4313594705 abstract "Ferroptosis is a currently recognized non-apoptotic cell death mode based on reactive oxygen species (ROS)-induced lipid peroxidation, which provides a promising strategy for cancer treatment. However, ferroptosis therapy has great challenges due to the low intracellular iron levels and the overexpressed lipid hydroperoxidase glutathione peroxidase 4 (GPX4). Here, we engineered a sequential pH/adenosine triphosphate (ATP)-sensitive nanomedicine by initially synthesizing zeolitic imidazolate framework 90 (ZIF90) containing metformin (Met) and RSL3 (Met/[email protected]) and then immobilizing it into iron ions and tannic acid (TA) integrated nanoscale coordination polymer (Fe-TA NCP) to obtain Met/[email protected]@Fe-TA. After entering the weakly acidic tumor microenvironment (TME), the structure of Fe-TA NCP was ruptured and the Met/[email protected] was exposed. The overexpressed ATP in cells could destroy the structure of the Met/[email protected] to release the loaded Met and RSL3. The freed iron ions catalyzed H2O2 via the Fenton reaction to promote the accumulation of lethal lipid peroxide (LPO). The exposed RSL3 through down-regulating glutathione peroxidase 4 (GPX4) broke the balance of GSH/GPX4, and the released Met activated the AMPK pathway to upregulate p53 and down-regulate SLC7A11. The results showed that the combination of continuous ferroptosis and apoptosis could lead to conspicuous cell death and significant tumor inhibition. Overall, this study paves a promoting strategy to improve the effectiveness of ferroptosis therapy by multipath destruction of antioxidant system." @default.
- W4313594705 created "2023-01-06" @default.
- W4313594705 creator A5014085938 @default.
- W4313594705 creator A5050438640 @default.
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- W4313594705 creator A5090730101 @default.
- W4313594705 date "2023-02-01" @default.
- W4313594705 modified "2023-10-17" @default.
- W4313594705 title "A pH/ATP-responsive nanomedicine via disrupting multipath homeostasis of ferroptosis for enhanced cancer therapy" @default.
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- W4313594705 doi "https://doi.org/10.1016/j.cej.2023.141313" @default.
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