ROS Self‐Supply Nanoplatform Based on Fenton Catalyst for Chemodynamic and Immunotherapy: Reprogramming Cold Tumor Into Hot Tumor in Cancer Treatment

ions deplete glutathione (GSH), further enhancing ROS accumulation. In vitro studies demonstrate that HA-PGMC induces significant ROS production, GSH depletion, lipid peroxidation, mitochondrial dysfunction, and robust antitumor effects with minimal toxicity to normal cells. Importantly, HA-PGMC triggers immunogenic cell death (ICD) by promoting CRT exposure and HMGB1 release, effectively converting "cold" tumors into "hot" tumors. This enhanced immune activation paves the way for synergistic combination with immune checkpoint blockade therapy. Collectively, this ROS-amplifying nanoplatform offers a promising strategy for overcoming the limitations of current cancer immunotherapy by simultaneously inducing potent chemodynamic therapy (CDT) and reprogramming the tumor immune microenvironment.