A lymph node-targeted nanoplatform reprograms metabolic and immune microenvironments via dual ACSL3/4 inhibition in lymphatic metastatic tumors.
Lymph node metastasis in hepatocellular carcinoma depends heavily on lipid metabolic reprogramming, wherein the acyl-CoA synthetase long-chain family members ACSL3 and ACSL4 act as central survival hubs. However, single-target interventions often fail to curb metastasis due to the inherent metabolic plasticity and flex...