Loading
Life sciences · Journal article
Small · November 4, 2026
No summary has been generated for this record yet. What follows is drawn from its source metadata only.
Journal article.
No findings were extractable from the material analysed.
Safety was not reported in the material analysed. Check the source before drawing any conclusion about harm.
The source did not state who this applies to in practice.
Graded across the dimensions that decide whether you should act, each from what the source actually supports. There is no single score, and where a dimension was not assessed it says so.
This record has not been graded across any dimension yet. Treat the label above as provisional and read the source.
What is missing. This record has no bottom line, key findings, reported figures, evidence dimensions. That is a gap in the analysis, not a judgement about the study.
ABSTRACT The malignant proliferation of tumors is driven by profound metabolic reprogramming, which offers a critical therapeutic target. However, conventional metabolic interventions are often limited by compensatory adaptation and off‐target toxicity. Here, we designed a tumor microenvironment triggered self‐reporting nanoplatform for metabolic blockade and cascade amplification of oxidative stress. The nanoplatform was constructed by co‐assembly of a trifluoromethyl‐grafted selenium‐containing histidine ( H SeF ) with Zn 2+ and encapsulation of the metabolic blocker, phenylboronic acid‐modified cholesterol (CholB). Once in the acidic tumor microenvironment, the nanoplatform disassembles to release Zn 2+ and CholB. Zn 2+ impairs mitochondrial function to generate a burst of reactive oxygen species (ROS), while CholB triggers Gaucher disease‐like lysosomal damage that is accompanied by depletion of polyamines (key endogenous antioxidants), thereby disabling a major cellular defense and amplifying oxidative stress. Meanwhile, redox switching of H SeF is transduced into a dual‐channel 19 F MRI signal, endowing the nanoplatform with a self‐reporting capability. In a 4T1 tumor model, the nanoplatform elicited dual immune activation (cGAS‐STING and immunogenic cell death) and achieved marked tumor suppression. This work offers a self‐reporting, activatable strategy that couples metabolic blockade with cascade‐amplified oxidative stress for dual immune activation, providing a promising approach for precision cancer therapy.