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. 2024 Mar 20;36:376–412. doi: 10.1016/j.bioactmat.2024.03.003

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© 2024 The Authors

This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).

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Fig. 11 — Nanomaterials modulating TAMs polarization for the treatment of HCC via iron metabolisms.

(A) DIC@M2pep-Fe-MOF effectively targets M2-type TAMs and promotes Hepcidin, thereby inhibiting ferroportin expression, reducing the iron efflux of M2-type TAMs, enhancing intracellular aggregation, and promoting M2-type macrophage polarization. M1-type TAMs promote CD8⁺ T cells and inhibit Tregs and MDSCs.

(B) Relative intracellular Fe content in M2-type macrophage after treatment with Dic@M2pep-FeMOF.

(C) Relative intracellular Fe content in M2-type macrophage after treatment with Dic@M2pep-FeMOF.

(D) Efficient repolarization of M2-type TAMs by Dic@M2pep-Fe-MOF in H22 tumor-bearing mice [204].Copyright 2021 Elsevier. TAMs, Tumor-associated macrophages; HCC, Hepatocellular carcinoma; Fe-MOF, Fe-Metal-organic framework; M2pep, M2 macrophage-binding peptide; Dic, Diclofenac; DIC@M2pep-Fe-MOF, Diclofenac encapsulated to M2pep-Fe-MOF; Tregs, Regulatory T cells; BMDCs, Bone marrow-derived myeloid cells.