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Preeclampsia (PE) is considered as a disease of placental origin. However, the specific mechanism of placental abnormalities remains elusive. This study identified thrombospondin‐1 (THBS1) is downregulated in preeclamptic placentae and negatively correlated with blood pressure. Functional studies show that THBS1 knockdown inhibits proliferation, migration, and invasion and increases the cycle arrest and apoptosis rate of HTR8/SVneo cells. Importantly, THBS1 silencing induces necroptosis in HTR8/SVneo cells, accompanied by the release of damage‐associated molecular patterns (DAMPs). Necroptosis inhibitors necrostatin‐1 and GSK′872 restore the trophoblast survival while pan‐caspase inhibitor Z‐VAD‐FMK has no effect. Mechanistically, the results show that THBS1 interacts with transforming growth factor B‐activated kinase 1 (TAK1), which is a central modulator of necroptosis quiescence and affects its stability. Moreover, THBS1 silencing up‐regulates the expression of neuronal precursor cell‐expressed developmentally down‐regulated 4 (NEDD4), which acts as an E3 ligase of TAK1 and catalyzes K48‐linked ubiquitination of TAK1 in HTR8/SVneo cells. Besides, THBS1 attenuates PE phenotypes and improves the placental necroptosis in vivo. Taken together, the down‐regulation of THBS1 destabilizes TAK1 by activating NEDD4‐mediated, K48‐linked TAK1 ubiquitination and promotes necroptosis and DAMPs release in trophoblast cells, thus participating in the pathogenesis of PE. The down‐regulation of THBS1 can destabilize TAK1 via NEDD4‐mediated, K48‐linked TAK1 ubiquitination, resulting in the activation of the necroptosis and DAMPs release in trophoblast cells, thus participating in the pathogenesis of PE.

Background Advancements in information technology, have made hospital information systems (HIS) essential tools for clinical nursing. The integration of HIS into undergraduate nursing education is a growing expectation within healthcare institutions. To meet this demand, nursing educators have promoted the incorporation of HIS into curricula to foster educational innovation. In response, our research team developed the Nursing Simulation Teaching Information System (NSTIS) to facilitate nursing operations related to HIS. We designed a comprehensive training course for senior students to prepare them for clinical rotations, with case simulations as a central component. This study aimed to assess the effectiveness of NSTIS in the training course and refine both the system and teaching scheme based on student feedback. Methods A total of 114 nursing students were assigned to either the experimental ( n  = 55) or the control group ( n  = 59), with only 114 students completing the intervention. Both groups worked on the same simulation case. The experimental group used the NSTIS to obtain complete medical records, whereas the control group used traditional Microsoft Word documents and printed materials. With informed consent from the participants, data were collected using a self-designed classroom teaching effect questionnaire and a case workshop scoring form. Results The experimental group scored higher than the control group on the total scores of the self-designed teaching effect questionnaire, with significant differences observed in specific items related to teaching objective achievement and learning outcomes. Qualitative data indicated that the experimental group reported acquiring skills in HIS operation. Both groups recommended adjustments to the teaching structure to enrich the case study resources, while the control group expressed a desire for measures to enhance their learning motivation. Conclusion Integrating NSTIS into a comprehensive training course can help enhance the effectiveness of case simulations. Further improvements to the NSTIS and teaching strategies are necessary for effective teaching. Future research should explore whether the application of the NSTIS in comprehensive training courses can improve students’ abilities and investigate how to integrate the NSTIS into other courses. Trial registration Not applicable.