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Autophagy, a lysosome‐involved degradation pathway, as a self‐protective cellular process, always weakens the efficiency of tumor therapies. Herein, for the first time, the biodegradable copper (Cu) ions doped layered double hydroxide (Cu‐LDH) nanoparticles are reported for cancer immunotherapy via lysosomal rupture‐mediated "Broken Window Effect". Only injection of Cu‐LDH single therapeutic agent achieves various organelles destruction after lysosomal rupture, as well as the abnormal aggregation of Cu ions in tumor cells for cuproptosis and pyroptosis. More importantly, autophagy inhibition caused by lysosomal rupture improves Cu ions overload‐mediated cuproptosis and pyroptosis by blocking the lysosome‐mediated bulk degradation pathway, leading to good anti‐tumor immune responses and ultimately high‐efficiency tumor growth inhibition. This lysosomal rupture‐mediated "Broken Window Effect" provides a new paradigm for the autophagy enhanced tumor therapy. [ABSTRACT FROM AUTHOR]

The layer‐by‐layer (LbL) organic photovoltaics (OPVs) are constructed with wide‐bandgap donor PM1 and narrow‐bandgap acceptor L8‐BO. The exciton utilization near cathode is still challenging considering restricted diffusion distance of excitons and inability for transferring energy from L8‐BO to PM1. Herein, donor incorporation into acceptor layer (DIA) strategy is employed to improve exciton utilization near cathode. The efficiency of LbL OPVs can be improved from 18.02% to 18.81% by incorporating 10 wt% PM1 into L8‐BO layer, which is closely associated with efficient exciton separation into L8‐BO layer originated from more adequate donor/acceptor interface for faster charge transfer, as evidenced by magneto‐photocurrent and transient absorption results. The in situ test and morphological characterization clarify that molecular packing property can be improved benefited from prolonged aggregation and nucleation time of acceptor layer assisted by DIA strategy, contributing to more efficient charge transport and inhibited charge recombination in active layers. The thickness insensitive property of LbL OPVs can be also improved induced by DIA strategy, indicated by PCE retention value (82.2% vs. 74.0%) for PM1/L8‐BO:PM1 and PM1/L8‐BO OPVs when acceptor layer thickness increased to ≈180 nm. This work demonstrates the effectiveness of DIA strategy in improving efficiency and thickness tolerance of LbL OPVs. [ABSTRACT FROM AUTHOR]

The aberrant metabolic activities of tumor cells not only facilitate tumor proliferation but also impair immune cell function and cause an immunosuppressive tumor microenvironment (TME). Thus, reshaping the metabolic TME while activating innate immunity is highly desirable but challenging. Herein, a multifunctional immunomodulator is engineered for near‐infrared light (NIR)‐triggered photodynamic‐metal‐metabolic immunotherapy via the “internal trouble and outside aggression” strategy. Specifically, an endogenous and exogenous stimuli‐responsive nanoagent is prepared consisting of photosensitizer chlorin e6 (Ce6) modified dense silica‐coated rare earth‐doped nanoparticles (ReNPs@SiO2(Ce6)), with in situ grown ZIF‐8 on the surface for loading glucose transporter‐1 (GLUT‐1) inhibitor Fasentin and glutaminase‐1 inhibitor bis‐2‐(5‐phenylacetamido‐1,3,4‐thiadiazol‐2‐yl)ethyl sulfide (BPTES). The as‐obtained final product is denoted as ReSZ(FB). ReSZ(FB) induces‐ mitochondrial damage and releases mitochondrial DNA (mtDNA) via NIR‐mediated PDT. Subsequently, Zn2+ from ZIF‐8 collaborates with mtDNA to activate the cGAS‐STING pathway, initiating a robust tumor‐specific immune response. Concurrently, Fasentin and BPTES triggeres energy deprivation by blocking glucose uptake and inhibiting glutamine decomposition, thereby reprogramming the metabolic TME, and alleviating immunosuppression. Tumor cells are damaged and trapped into “internal trouble” by combining PDT and energy deprivation, while the sharply enhanced immune cell lethality exposes cancer cells to “outside aggression”. Overall, this photodynamic‐metal‐metabolic immunotherapy provides a promising paradigm for cancer therapy. [ABSTRACT FROM AUTHOR]