已传文件：photo/1773121782.png
The article reported by Cheng Liang from Soochow University and Ni Caifang from Soochow University Affiliated First Hospital is not merely another "embolization and drug release" microsphere, but it truly addresses the core clinical contradiction of why liver cancer always resurges after TACE/TAE: embolization, on the one hand, cuts off the blood supply and causes hypoxia, which can suppress the tumor in the short term; but on the other hand, hypoxia will quickly activate HIF-1α/VEGF-driven compensatory angiogenesis and force the tumor to switch to a stronger glycolytic metabolism, with lactate accumulation further shaping an immunosuppressive microenvironment, ultimately turning "local ischemic attack" into "tumor adaptive upgrade".
The authors have constructed a ZnS@GMs dual-targeting microsphere system: using gelatin microspheres as the embolization carrier, H₂S and Zn²⁺ are continuously released in the acidic embolization environment of the tumor microenvironment. Among them, H₂S is not merely a simple gimmick for gas therapy, but is used to inhibit mitochondrial respiration, increase local oxygen availability, thereby destabilizing HIF-1α, lowering VEGF, alleviating abnormal hypoxia and promoting vascular normalization; Zn²⁺ is more inclined to "starvation", directly inhibiting key enzymes of glycolysis such as HK and LDH, lowering glucose consumption, lactate production and ATP supply, and cutting off the most important metabolic escape pathway of the tumor after embolization. That is to say, this system is not a single killing action, but acts simultaneously on two lines: anti-angiogenesis + anti-glycolytic reprogramming. The related research, titled "Dual-targeted microspheres reshape the metabolic-immune microenvironment to reverse post-embolization dilemmas in hepatocellular carcinoma", was published in Cell Reports Medicine.
