Taming Reactive Oxygen Species: Mitochondria-Targeting Aggregation-Induced Emission Luminogen for Neuron Protection via Photosensitization-Triggered Autophagy

Oxidative damage to cells leads to accumulated harmful wastes, which in turn aggravate the imbalance of reactive oxygen species (ROS) and related diseases. Therefore, provoking the cellular defense system against severe oxidation and maintaining ROS homeostasis are desired. Herein, we designed and synthesized a powerful mitochondria-targeting aggregation-induced emission photosensitizer (named DTCSPY) by maximal restriction of heat dissipation. It is demonstrated that taming ROS generation within mitochondria through photosensitization-triggered autophagy via DTCSPY achieved a better neuroprotective effect against oxidative damages than Nacety-L-cysteine and vitamin C. This work not only provides a new way to design high-performance photosensitizers by regulating the photophysical property, but also verifies the concept that taming ROS can be used for cell protection against destructive oxidation, thereby displaying broad prospects for alleviating oxidation-related diseases and promoting cell-based therapy. [GRAPHICS]

Automated summary

This study designed and synthesized a mitochondria-targeting aggregation-induced emission photosensitizer (DTCSPY), which achieved a better neuroprotective effect by inhibiting ROS generation through photosensitization-triggered autophagy. It provides a new approach for designing high-performance photosensitizers.