Shape Memory Polymer Composites:4D Printing,Smart Structures,and Applications

Shape memory polymers (SMPs) and their composites (SMPCs) are smart materials that can be stably deformed and then return to their original shape under external stimulation, thus having a memory of their shape. Three-dimensional (3D) printing is an advanced technology for fabricating products using a digital software tool. Four-dimensional (4D) printing is a new generation of additive manufacturing technology that combines shape memory materials and 3D printing technology. Currently, 4D-printed SMPs and SMPCs are gaining considerable research attention and are finding use in various fields, including biomedical science. This review introduces SMPs, SMPCs, and 4D printing technologies, highlighting several special 4D-printed structures. It summarizes the recent research progress of 4D-printed SMPs and SMPCs in various fields, with particular emphasis on biomedical applications. Additionally, it presents an overview of the challenges and development prospects of 4D-printed SMPs and SMPCs and provides a preliminary discussion and useful reference for the research and application of 4D-printed SMPs and SMPCs.

Auranofin mitigates systemic iron overload and induces ferroptosis via distinct mechanisms

Iron homeostasis is essential for health;moreover,hepcidin-deficiency results in iron overload in both hereditary hemochromatosis and iron-loading anemia.Here,we identified iron modulators by functionally screening hepcidin agonists using a library of 640 FDA-approved drugs in human hepatic Huh7 cells.We validated the results in C57BL/6J mice and a mouse model of hemochromatosis(Hfe^(−/−)mice).Our screen revealed that the anti-rheumatoid arthritis drug auranofin(AUR)potently upregulates hepcidin expression.Interestingly,we found that canonical signaling pathways that regulate iron,including the Bmp/Smad and IL-6/Jak2/Stat3 pathways,play indispensable roles in mediating AUR’s effects.In addition,AUR induces IL-6 via the NF-κB pathway.In C57BL/6J mice,acute treatment with 5 mg/kg AUR activated hepatic IL-6/hepcidin signaling and decreased serum iron and transferrin saturation.Whereas chronically treating male Hfe^(−/−)mice with 5 mg/kg AUR activated hepatic IL-6/hepcidin signaling,decreasing systemic iron overload,but less effective in females.Further analyses revealed that estrogen reduced the ability of AUR to induce IL-6/hepcidin signaling in Huh7 cells,providing a mechanistic explanation for ineffectiveness of AUR in female Hfe^(−/−)mice.Notably,high-dose AUR(25 mg/kg)induces ferroptosis and causes lipid peroxidation through inhibition of thioredoxin reductase(TXNRD)activity.We demonstrate the ferroptosis inhibitor ferrostatin significantly protects liver toxicity induced by highdose AUR without comprising its beneficial effect on iron metabolism.In conclusion,our findings provide compelling evidence that TXNRD is a key regulator of ferroptosis,and AUR is a novel activator of hepcidin and ferroptosis via distinct mechanisms,suggesting a promising approach for treating hemochromatosis and hepcidin-deficiency related disorders.

Amine-functionalized SiO2 nanodot-coated layered double hydroxide nanocomposites for enhanced gene delivery

In this work a novel strategy has been developed to prepare well-dispersed amine-functionalized SiO2 nanodot-coated layered double hydroxide nano- composite （NH2-SiO2@LDH） via electrostatic interactions and condensation of （3-aminopropyl）triethoxysilane （APTES）. This nanocomposite system is well dispersed in culture media and phosphate buffered saline, and exhibits low cytotoxicity and good biocompatibility. The fluorescence microscopy images and flow cytometry data indicate that such an NH2-SiO2@LDH nanocomposite is able to efficiently deliver small interfering RNA （siRNA） into the U2OS cell line to inhibit cell proliferation. Thus, NH2-SiOR@LDH nanocomposite has a great potential as a nanocarrier for efficient gene delivery.