2D Catalytic Nanozyme Enables Cascade Enzyodynamic Effect-Boosted and Ca2+ Overload-Induced Synergistic Ferroptosis/Apoptosis in Tumor.
Adv Mater
; 36(24): e2312316, 2024 Jun.
Article
en En
| MEDLINE
| ID: mdl-38501540
ABSTRACT
The introduction of glucose oxidase, exhibiting characteristics of glucose consumption and H2O2 production, represents an emerging antineoplastic therapeutic approach that disrupts nutrient supply and promotes efficient generation of reactive oxygen species (ROS). However, the instability of natural enzymes and their low therapeutic efficacy significantly impede their broader application. In this context, 2D Ca2Mn8O16 nanosheets (CMO NSs) designed and engineered to serve as a high-performance nanozyme, enhancing the enzyodynamic effect for a ferroptosis-apoptosis synergistic tumor therapy, are presented. In addition to mimicking activities of glutathione peroxidase, catalase, oxidase, and peroxidase, the engineered CMO NSs exhibit glucose oxidase-mimicking activities. This feature contributes to their antitumor performance through cascade catalytic reactions, involving the disruption of glucose supply, self-supply of H2O2, and subsequent efficient ROS generation. The exogenous Ca2+ released from CMO NSs, along with the endogenous Ca2+ enrichment induced by ROS from the peroxidase- and oxidase-mimicking activities of CMO NSs, collectively mediate Ca2+ overload, leading to apoptosis. Importantly, the ferroptosis process is triggered synchronously through ROS output and glutathione consumption. The application of exogenous ultrasound stimulation further enhances the efficiency of ferroptosis-apoptosis synergistic tumor treatment. This work underscores the crucial role of enzyodynamic performance in ferroptosis-apoptosis synergistic therapy against tumors.
Palabras clave
Texto completo:
1
Colección:
01-internacional
Banco de datos:
MEDLINE
Asunto principal:
Calcio
/
Especies Reactivas de Oxígeno
/
Apoptosis
/
Ferroptosis
Límite:
Animals
/
Humans
Idioma:
En
Revista:
Adv Mater
Asunto de la revista:
BIOFISICA
/
QUIMICA
Año:
2024
Tipo del documento:
Article