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La administración de sulfuro de hidrógeno mediada por enzimas de un solo átomo de hierro amplifica la cascada de

Xuegang Niu^1,2,3, Penghui Wei^1,2, Mingtao Zhu^1,4

¹Department of Neurosurgery, Neurosurgery Research Institute, The First Affiliated Hospital, Fujian Medical University, Fuzhou, Fujian, 350005, China.

Materials today. Bio

|August 21, 2025

Resumen

Este estudio introduce una nueva nanoplataforma enzimática de un solo átomo de hierro (Fe/SAE@A) que mejora la ferroposis en las células cancerosas. Entrega sulfuro de hidrógeno (H2S) para inhibir la eliminación de ROS, amplificando la peroxidación lipídica y la muerte de las células cancerosas.

Área de la Ciencia:

Ingeniería biomédica
Nanotecnología
Investigación del cáncer

Sus antecedentes:

La peroxidación lipídica (LPO) es un factor clave en la susceptibilidad a la ferroposis.
Los microambientes tumorales a menudo poseen altos niveles de glutatión (GSH) y enzimas de eliminación de ROS, lo que dificulta la ferroposis.
Dirigirse a estos mecanismos protectores es crucial para una terapia eficaz contra el cáncer.

Objetivo del estudio:

Desarrollar una nanoplataforma que amplifique la vulnerabilidad a la ferroptosis mediada por LPO en las células cancerosas.
Investigar los efectos sinérgicos del sulfuro de hidrógeno (H2S) y las enzimas de un solo átomo de hierro (Fe/SAE) en el tratamiento del cáncer.
Para explorar una nueva estrategia para superar la resistencia del tumor a la ferroptosis.

Principales métodos:

Desarrollo de una nanoplataforma Fe/SAE (Fe/SAE@A) capaz de suministrar tritión de anetol (ADT) como donante de H2S.
Utilizando la actividad de imitación de la peroxidasa de Fe/SAE para generar radicales hidroxilo a partir de H2O2.
Investigación de la inhibición de las enzimas de eliminación de ROS y la oxidación de GSH por H2S y Fe/SAE@A.

Principales resultados:

Fe/SAE@A proporciona efectivamente H2S, inhibiendo las enzimas que eliminan ROS y aumentando los niveles intracelulares de H2O2.
Fe/SAE cataliza una cascada de ROS, lo que lleva a una LPO irreversible y una ferroptosis mejorada.
Fe/SAE@A también exhibe actividad de la glutationa oxidasa, agotando la GSH e inactivando la GPX4.

Conclusiones:

La nanoplataforma Fe/SAE@A potencia la ferroposis mediante la entrega de H2S, induciendo una tormenta de ROS y consumiendo GSH.
Esta estrategia mejora efectivamente la susceptibilidad de las células cancerosas a la ferroposis, ofreciendo un enfoque terapéutico prometedor.
Aprovechar las enzimas monoatómicas en cascada que liberan H2S presenta una nueva vía para la terapia del cáncer.

Palabras clave:

Tratamiento catalítico La ferroposis Sulfuro de hidrógeno Especies reactivas de oxígeno Enzima de un solo átomo

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