With the rapid development of lithium‐ion batteries (LIBs), safety problems are the great obstacles that restrict large‐scale applications of LIBs, especially for the high‐energy‐density electric vehicle industry. Developing component materials (e.g., cathode, anode, electrolyte, and separator) with high thermal stability and intrinsic safety is the ultimate solution to improve the safety of LIBs. Separators are crucial components that do not directly participate in electrochemical reactions during charging/discharging processes, but play a vital role in determining the electrochemical performance and safety of LIBs. In this review, the recent advances on traditional separators modified with ceramic materials and multifunctional separators ranging from the prevention of the thermal runaway to the flame retardant are summarized. The component–structure–performance relationship of separators and their effect on the comprehensive performance of LIBs are discussed in detail. Furthermore, the research challenges and future directions toward the advancement in separators for high‐safety LIBs are also proposed.

Endometriosis is an estrogen-dependent benign gynecological disease that shares some common features of malignancy. Epithelialmesenchymal transition (EMT) has been recognized as a core mechanism of endometriosis. MALAT1 is widely known as EMT promoter, while miR200 family members (miR200s) are considered as EMT inhibitors. Previous studies have reported that MALAT1 upregulation and miR200s downregulation are observed in endometriosis. MiR200c has been regarded as the strongest member of miR200s to interact with MALAT1. However, whether MALAT1/miR200c regulates EMT remains largely unclear. In this study, the roles of miR200s and MALAT1 in ectopic endometrium were investigated. Additionally, the effects of E 2 on EMT and MALAT1/ miR200s were examined in both EECs and Ishikawa cells. Notably, E 2 could upregulate MALAT1 and downregulate miR200s expression levels and induce EMT in EECs and Ishikawa cells. PHTPP, an ERβ antagonist, could reverse the effect of E 2 . Overexpression of miR200c and knockdown of MALAT1 significantly inhibited E 2 -mediated EMT, suggesting that both miR200c and MALAT1 are involved in the E 2 -induced EMT process in endometriosis. In addition, a reciprocal inhibition was found between miR200s and MALAT1. Therefore, the role of MALAT1/miR200c in EMT is influenced by the presence of estrogen during endometriosis development.Reproduction (2019) 157 179-188

NOD-like receptor family, pyrin domain-containing protein 3 (NLRP3) inflammasome-mediated pyroptosis is a crucial event in the preeclamptic pathogenesis, tightly linked with the uteroplacental TLR4/NF-κB signaling. Trophoblastic glycometabolism reprogramming has now been noticed in the preeclampsia pathogenesis, plausibly modulated by the TLR4/NF-κB signaling as well. Intriguingly, cellular pyroptosis and metabolic phenotypes may be inextricably linked and interacted. Metformin (MET), a widely accepted NF-κB signaling inhibitor, may have therapeutic potential in preeclampsia while the underlying mechanisms remain unclear. Herein, we investigated the role of MET on trophoblastic pyroptosis and its relevant metabolism reprogramming. The safety of pharmacologic MET concentration to trophoblasts was verified at first, which had no adverse effects on trophoblastic viability. Pharmacological MET concentration suppressed NLRP3 inflammasome-induced pyroptosis partly through inhibiting the TLR4/NF-κB signaling in preeclamptic trophoblast models induced via low-dose lipopolysaccharide. Besides, MET corrected the glycometabolic reprogramming and oxidative stress partly via suppressing the TLR4/NF-κB signaling and blocking transcription factor NF-κB1 binding on the promoter PFKFB3, a potent glycolytic accelerator. Furthermore, PFKFB3 can also enhance the NF-κB signaling, reduce NLRP3 ubiquitination, and aggravate pyroptosis. However, MET suppressed pyroptosis partly via inhibiting PFKFB3 as well. These results provided that the TLR4/NF-κB/PFKFB3 pathway may be a novel link between metabolism reprogramming and NLRP3 inflammasome-induced pyroptosis in trophoblasts. Further, MET alleviates the NLRP3 inflammasome-induced pyroptosis, which partly relies on the regulation of TLR4/NF-κB/PFKFB3-dependent glycometabolism reprogramming and redox disorders. Hence, our results provide novel insights into the pathogenesis of preeclampsia and propose MET as a potential therapy.