Abstract
Mitochondria, as one of the most critical subcellular organelles of cancer cells, are very vulnerable and often on the verge of oxidative stress. The classic chemodynamic therapy (CDT) directly employs endogenous chemical energy to trigger reactive oxygen species (ROS) burst and destroy tumor cells. However, the effectiveness of CDT is restricted by the limited diffusion distance and short half-life of ROS. From this perspective, the treatment method (mitochondria-targeting chemodynamic therapy nanodrugs, M-CDT nanodrugs) that can generate high levels of ROS at the mitochondrial site is extremely efficient and promising for cancer treatment. Currently, many emerging M-CDT nanodrugs have been demonstrated excellent spatial specificity and anti-cancer efficacy. In this minireview, we review various proof-of-concept researches based on different M-CDT nanodrugs designs to overcome the limits of the efficacy of CDT, mainly divided into four strategies: supplying H2O2, non-H2O2 dependent CDT, eliminating GSH and enhancing by hyperthermia therapy (HT). These well-designed M-CDT nanodrugs greatly increase the efficacy of CDT. Finally, the progress and potential of M-CDT nanodrugs are discussed, as well as their limitations and opportunities.
Highlights
Many new therapeutic targets and emerging therapies have been developed to find the Achilles heel of cancer cells (de Lázaro and Mooney, 2021)
We review various proof-of-concept researches based on different M-chemodynamic therapy (CDT) nanodrugs designs to overcome the limits of the efficacy of CDT, mainly divided into four strategies: supplying H2O2, non-H2O2 dependent CDT, eliminating GSH and enhancing by hyperthermia therapy (HT)
Traditional anticancer drugs including CDT agents are limited by their poor pharmacokinetic properties, such as low bioavailability, short half-life and low stability
Summary
Many new therapeutic targets and emerging therapies have been developed to find the Achilles heel of cancer cells (de Lázaro and Mooney, 2021). The mitochondria of cancer cells usually undergo metabolic reprogramming for rapid proliferation and invasion, that is, they are more inclined to glycolysis than oxidative phosphorylation to produce ATP (Martínez-Reyes and Chandel, 2021). This process produces a higher level of reactive oxygen species (ROS), which makes the mitochondria themselves on the verge of oxidative stress CDT agents with targeting mitochondria can produce a high level of ROS in situ on mitochondria to cause severely mitochondrial damage and further trigger cell death (Zeng et al, 2021). The therapeutic efficacy of M-CDT nanodrugs is further increased by GSH depletion (Wang et al, 2021b), H2O2 supplementation (Sun et al, 2021), non-H2O2 dependent CDT (Zhang et al, 2019), and combination hyperthermia
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