Abstract
Macrophages,as a subset of innate immune cells,play a pivotal role in the initiation,maintenance,and resolution of inflammatory responses during tissue damage repair,defense against infections,and tumor progression.However,the mechanisms by which macrophages regulate inflammation in acute myeloid leukemia(AML)and their involvement in the chemotherapeutic effect remain elusive.In this study,we have identified that AML cells stimulate macrophage expansion by activating the colony-stimulating fac-tor 1 receptor(CSF1R)pathway.The expanded macrophages activate nuclear factor kappa-B(NFκB)to induce the expression of inflammatory factors,thereby maintaining leukemic cell quiescence and pro-moting cell survival following chemotherapy.Furthermore,we have successfully utilized a poly(ferulic acid)nanocarrier to selectively target macrophages for inhibiting the NFκB-mediated inflammation,ulti-mately enhancing chemotherapy efficacy against AML.Taken together,our findings highlight the crucial role of macrophage-induced inflammation in conferring chemoresistance to AML,and demonstrate the potential of a targeted nanocarrier specifically designed for inflammatory macrophages to improve the AML chemotherapeutic outcomes.
维普
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