Gold nanomaterials have been used in the diagnosis and treatment of different tumors due to their unique physical and chemical properties. Among them, gold nanoparticles with stimuli‐responsive aggregation functions have attracted extensive attention because they can meet the unique needs of tumor diagnosis and treatment at different stages through structural changes. However, how to effectively modify gold nanoparticles to achieve structural transformation for specific stimuli, and the role of corresponding structural transformation in improving the effect of diagnosis and treatment still lack systematic summary. In this review, we comprehensively summarized the current strategies for inducing gold nanoparticles aggregation and its advances in tumor diagnosis and treatment.

Alterations in the gut microbiota are among the most common phenomena following spinal cord injury, often accompanied by cognitive impairment. Numerous studies have reported intrinsic links among these three aspects. However, the molecular mechanisms by which the gut microbiota influence cognitive function after spinal cord injury, as well as strategies for modulating the gut microbiota to treat cognitive deficits, remain inadequately summarized. Therefore, this review provides a comprehensive summary of the key mechanisms by which gut dysbiosis contributes to cognitive impairment and discusses therapeutic strategies targeting the gut microbiota. These insights may offer a theoretical basis for further research and microbiota-based drug development for cognitive dysfunction following spinal cord injury.

Spatiotemporally controlled reactive oxygen species (ROS) generation remains pivotal for advancing photodynamic immunotherapy. Herein, we present tumor microenvironment (TME)-responsive nano-immunoregulator featuring a CaCO₃ shell encapsulating a mesoporous silica core modified with folic acid/chlorin e6 (FA/Ce6) and co-loaded with dBET6 and maleimide (MA). Acidic TME triggers CaCO₃ shell degradation, neutralizing tumor acidity to repolarize macrophages toward M1 type, enhancing antigen presentation and T cells immune response while exposing the BM@M_FC core. The resulting BM@M_FC further endocytosed by tumor cells via FA-mediated tumor targeting, followed by MA-mediated glutathione depletion amplifies Ce6-generated ROS for potent photodynamic therapy (PDT). Concurrently, dBET6 degrades BRD4 to inhibit metastasis, downregulate PD-L1, and synergize with PDT to induce immunogenic cell apoptosis, thereby activating dendritic cells (DCs) and T cells for enhanced photodynamic immunotherapy. Both in vitro/vivo results indicate that BM@M_FCC have excellent performance to inhibit primary/metastatic tumors, while single-cell RNA sequencing elucidates BM@M_FCC can induce immunosuppressive TME remodeling, including increased CD8⁺ T cells, cDCs, and NK cells; M2-to-M1 macrophage polarization; and enhanced intercellular communication. Tumor cell profiling confirms BM@M_FCC will downregulate oncogenic pathways and activate immune signatures. Collectively, this TME responsive nano-immunoregulator demonstrates superior therapeutic outcomes and provides a promising strategy for precision cancer photodynamic immunotherapy.