Implantation of occlusion devices is an effective approach for the treatment of congenital heart diseases in the clinic. However, most commercial clinical occlusion devices are currently made of nondegradable metals, which may lead to complications such as perforation, allergies, and erosion. In this work, 4D-printed novel, biodegradable, remotely controllable, and personalized shape memory occlusion devices are demonstrated and atrial septal defect occluders are exemplified. By incorporating Fe 3 O 4 magnetic particles into the shape memory poly(lactic acid) matrix, the deployment of the occluders can be controlled remotely after implantation. The excellent cytocompatibility and histocompatibility are conducive to cell adhesion and ingrowth of granulation tissues into the occluders, thus facilitating rapid endothelialization. In addition, personalized shape memory occluders ensure an ideal fit and provide sufficient support for defects. Therefore, 4D-printed shape memory occluders can be used as a potential substitute for metal occlusion devices.
Treatment with doxorubicin (DOX) is one of the major causes of chemotherapy-induced cardiotoxicity and is therefore, the principal limiting factor in the effectiveness of chemotherapy for cancer patients. DOX‑induced heart failure is thought to result from endoplasmic reticulum (ER) stress and cardiomyocyte apoptosis. Resveratrol (RV), a polyphenol antioxidant found in red wine, has been shown to play a cardioprotective role. The aim of the present study was to examine the effects of RV on DOX‑induced cardiotoxicity in H9c2 cells. We hypothesized that RV would protect H9c2 cells against DOX‑induced ER stress and subsequent cell death through the activation of the Sirt1 pathway. Our results demonstrated that the decrease observed in the viability of the H9c2 cells following exposure to DOX was accompanied by a significant increase in the expression of the ER stress‑related proteins, glucose‑regulated protein 78 (GRP78) and C/EBP homologous protein (CHOP). However, we found that RV downregulated the expression of ER stress marker protein in the presence of DOX and restored the viability of the H9c2 cells. Exposure to RV or DOX alone only slightly increased the protein expression of Sirt1, whereas a significant increase in Sirt1 protein levels was observed in the cells treated with both RV and DOX. The Sirt1 inhibitor, nicotinamide (NIC), partially neutralized the effects of RV on the expression of Sirt1 in the DOX‑treated cells and completely abolished the effects of RV on the expression of GRP78 and CHOP. The findings of our study suggest that RV protects H9c2 cells against DOX‑induced ER stress through ER stabilization, and more specifically through the activation of the Sirt1 pathway, thereby leading to cardiac cell survival.
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