Therapeutic Potential of Carbon Dots Derived from Phytochemicals as Nanozymes Exhibiting Superoxide Dismutase Activity for Anemia

Anemia is a potentially life-threatening blood disorder caused by an insufficient erythroblast volume in the circulatory system. Self-renewal failure of erythroblast progenitors is one of the key pathological factors leading to erythroblast deficiency. However, there are currently no effective drugs that selectively target this process. In this work, we present a carbon dot (CP-CDs) derived from phytochemicals that significantly promotes the self-renewal of erythroblast progenitors for anemia therapy. As a superoxide dismutase (SOD)-like nanozyme, CP-CDs significantly activate the hypoxia response and JAK/STAT3 pathways in erythroid cells by reprogramming the oxidative stress state. This results in unique erythropoiesis-enhancing properties by promoting the generation of erythroid progenitor cells. Moreover, CP-CDs protect mature red blood cells by inhibiting oxidative stress-induced damage and improving the immune-inflammatory microenvironment. In vivo, CP-CDs showed a promising therapeutic effect in mouse and zebrafish models of anemia with minimal adverse effects, indicating significant translational medical value. Collectively, this study not only illustrates a successful approach for nanomedicine-enhanced anemia therapy but also enhances our understanding of the interaction between nanomedicine and the self-renewal of erythroblast progenitors.