Cryptotanshinone (CT) is a diterpene quinone compound from Salvia miltiorrhiza Bge. Labiatae has been widely used in cardio-cerebral vascular diseases, which could be potentially effective in treat...

Ferroptosis is an iron-dependent form of regulated cell death characterized by the accumulation of iron-dependent lipid peroxides, which has been implicated in the pathogenesis of various diseases, and therapeutic agents targeting ferroptosis are emerging as promising tools for cancer treatment. Current research reveals that ferroptosis-targeted therapies can effectively inhibit tumor progression or delay cancer development. Notably, natural product-derived compounds—such as artemisinin, baicalin, puerarin, quercetin, kaempferol, and apigenin—have demonstrated the ability to modulate ferroptosis, offering potential anti-cancer benefits. Mechanistically, ferroptosis exhibits negative glutathione peroxidase 4 (GPX4) regulation and demonstrates a positive correlation with plasma membrane polyunsaturated fatty acid (PUFA) abundance. Moreover, the labile iron pool (LIP) serves as the redox engine of ferroptosis. This review systematically analyzes the hallmarks, signaling pathways, and molecular mechanisms of ferroptosis, with a focus on how natural product-derived small molecules regulate this process. It further evaluates their potential as ferroptosis inducers or inhibitors in anti-tumor therapy, providing a foundation for future clinical translation.

MDSCs are immature myeloid immune cells, which accumulate in models of liver cancer to reduce effector immune cell activity, contribute to immune escape and treatment resistance. The accumulation of MDSCs suppresses the role of CTL and the killing effects of NK cells, induces the accumulation of Treg cells, and blocks the antigen presentation of DCs, thus promoting the progression of liver cancer. Recently, immunotherapy has emerged a valuable approach following chemoradiotherapy in the therapy of advanced liver cancer. A considerable increasing of researches had proved that targeting MDSCs has become one of the therapeutic targets to enhance tumor immunity. In preclinical study models, targeting MDSCs have shown encouraging results in both alone and in combination administration. In this paper, we elaborated immune microenvironment of the liver, function and regulatory mechanisms of MDSCs, and therapeutic approaches to target MDSCs. We also expect these strategies to supply new views for future immunotherapy for the treatment of liver cancer.