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. 2023 Mar 21;13(6):1974–2014. doi: 10.7150/thno.80887

Figure 1.

Figure 1

(A) Schematic illustration of the construction of a) iHMNCPt-O2 nanoplatform and b) the pathways on which it acts to synergistically accelerate cancer death by combining CDT with chemotherapy. Reproduced with permission 56. Copyright 2020, American Chemical Society. (B) Schematic illustration of a) the intracellular copper metabolism route mediated by GSH and b) the biomimic mechanism of the β-lapa@CuPMs therapy route in tumor cells. Reproduced with permission 57. Copyright 2021, American Chemical Society. (C) a) The cartoon illustration and chemical structures of the building blocks (TCPP(Fe), PEG-SH, C12SH, and CPT). b) Preparation of the hybrid nanomedicine PEG-Au/FeMOF@CPT. c) High tumor accumulation of PEG-Au/FeMOF@CPT NPs via passive targeting and subsequently cancer cell uptake. Triggered by the intracellular phosphate, the chemotherapeutic drug CPT is released and the cascade catalytic reactions are activated. H2O2 generated through the oxidation of glucose by Au NPs acts as chemical fuel for Fenton reaction to produce highly toxic ROS to realize chemo/chemodynamic therapy. Reproduced under the terms of the http://creativecommons.org/licenses/by/4.0/ License 59, published by WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim. (D) Schematic illustration of the preparation of G5.NHAc-Toy@TF nanocomplexes for MR imaging and chemotherapy/CDT of tumors in vivo through ERS amplification. Reproduced with permission 61. Copyright 2021, Wiley-VCH.