This research demonstrates enhanced tumor apoptosis through nanocatalytic oxidative stress amplification in mitochondria, implying a novel therapeutic strategy.
Key Points
This study aims to improve tumor treatment using a nanotherapeutic platform that targets mitochondria to amplify oxidative stress and disrupt mitophagy.
Developed mitochondria-targeted nanotherapeutic platform with cobalt single-atom nanocatalysts functionalized with triphenylphosphine and chloroquine.
Localized nanocatalysts in mitochondria for enhanced oxidative stress generation.
Measured the impact of oxidative stress on mitochondrial electron transport chain function and mitophagy.
Nanocatalysts generated superoxide anions and molecular oxygen, leading to amplified oxidative stress.
Disruption of the electron transport chain was observed, enhancing oxidative stress.
Chloroquine effectively inhibited mitophagy, allowing accumulation of dysfunctional mitochondria, which increased tumor cell apoptosis.