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Constructing hierarchical porosity and designing rational hybrid composition are effective strategies for enhancing the electrocatalytic performance of hybrid catalysts for electrochemical energy conversion. Here, we develop a multistep “molecule/ion-exchange” strategy toward the synthesis of hierarchically macro/mesoporous Fe,Ni-doped CoSe/N-doped carbon nanoshells with tunable pore structures and compositions. Polystyrene (PS)@Co-based amorphous coordination polymer (Co-CP) core–shell particles with hierarchically macro/mesoporous nanoshells are first prepared by ligand-molecule-exchange etching of the outer layers in PS@Co-based metal–organic framework precursors. Afterward, a liquid–solid dual-ion-exchange reaction of PS@Co-CP particles with [Fe­(CN)6]3– and [Ni­(CN)4]2– ions leads to the formation of PS@Co-CP/Co–Fe Prussian blue analogue (PBA)/Co–Ni PBA particles, which are further transformed into hierarchically macro/mesoporous Fe,Ni-doped CoSe/N-doped carbon particles via a vapor–solid selenization reaction. Moreover, this approach could be extended to synthesize different hierarchically porous core–shell composites with various morphologies and tailored compositions. Because of their unique hierarchically porous nanoarchitecture, these Fe,Ni-doped CoSe/N-doped carbon particles with optimized composition show enhanced performance for electrocatalytic oxygen evolution.

Background The induction of pyroptosis holds great promise as a strategy for improving the tumor immune microenvironment. Previous pyroptosis inducers have faced limitations, including drug resistance, toxic side effects, and a lack of targeting capabilities. As a result, there is a growing demand for tumor therapeutic molecules that can overcome these obstacles. With this in mind, the objective of this study is to develop a multifunctional nanospheres that addresses these challenges by enabling high-precision targeting of tumor cells and effective pyroptosis induction. Results We prepared a mannose-modified MOF called mannose-doped Fe3O4@NH2-MIL-100, referred to as M-FNM. M-FNM has the ability to enter CAL27 cells through MR-mediated endocytosis, which results in a significant increase in intracellular ROS levels. This increase subsequently triggers endoplasmic reticulum stress (ER stress) and activates the PERK-eIF2α-ATF4-CHOP signaling pathway. CHOP then mediates the downstream cascade of Caspase-1, inducing pyroptosis. In in vivo experiments, M-FNM demonstrates excellent targeting ability and exhibits anti-tumor effects. Additionally, M-FNM reshapes the immune microenvironment by promoting the infiltration of anti-tumor immune cells, primarily T lymphocytes. Conclusions M-FNM significantly decreased tumor growth. This novel approach of inducing pyroptosis in tumor cells using M-FNM may offer new avenues for the development of effective immunotherapies for cancer treatment.