An esterase-activated celastrol delivery system suppressed steatosis-related hepatocellular carcinoma progression

studies showed that the lipid degradation efficacy of PQDMA@CEL NPs was 1.8-fold higher than that of free CEL in steatotic hepatocellular AML12 cells. In the Hepa1-6 bilateral tumor model, a single-site intratumoral injection of PQDMA@CEL NPs systemically boosted the anticancer efficacy. The tumor inhibition rate of PQDMA@CEL NPs was 72.4% for treated tumors and 65.8% for the distant untreated tumors. In summary, this approach provides new insights into the inhibition of steatosis-related HCC progression by inducing ferroptosis and decreasing lipid accumulation in HCC.