All-solid-state lithium batteries are promising next-generation energy storage devices that have gained increasing attention in the past decades due to their huge potential towards higher energy density and safety. As a key component, solid electrolytes have also attracted significant attention and have experienced major breakthroughs, especially in terms of Li-ion conductivity. However, the poor electrode compatibility of solid electrolytes can lead to the degradation of electrolyte/electrode interfaces, which is the major cause for failure in all-solid-state lithium batteries. To address this, this review will summarize the indepth understanding of physical and chemical interactions between electrolytes and electrodes with a focus on the contact, charge transfer and Li dendrite formation occurring at electrolyte/electrode interfaces. Based on mechanistic analyses, this review will also briefly present corresponding strategies to enhance electrolyte/electrode interfaces through compositional modifications and structural designs. Overall, the comprehensive insights into electrolyte/electrode interfaces provided by this review can guide the future investigation of all-solid-state lithium batteries.

Nicorandil exerts myocardial protection through its antihypoxia and antioxidant effects. Here, we investigated whether it plays an anti‐apoptotic role in diabetic cardiomyopathy. Sprague‐Dawley rats were fed with high‐fat diet; then single intraperitoneal injection of streptozotocin was performed. Rats with fasting blood glucose (FBG) higher than 11.1 mmol/L were selected as models. Eight weeks after the models were built, rats were treated with nicorandil (7.5 mg/kg day and 15 mg/kg day respectively) for 4 weeks. H9c2 cardiomyocytes were treated with nicorandil and then stimulated with high glucose (33.3 mmol/L). TUNEL assay and level of bcl‐2, bax and caspase‐3 were measured. 5‐HD was used to inhibit nicorandil. Also, PI3K inhibitor (Miltefosine) and mTOR inhibitor (rapamycin) were used to inhibit PI3K/Akt pathway. The results revealed that nicorandil (both 7.5 mg/kg day and 15mg/kg day) treatment can increase the level of NO in the serum and eNOS in the heart of diabetic rats compared with the untreated diabetic group. Nicorandil can also improve relieve cardiac dysfunction and reduce the level of apoptosis. In vitro experiments, nicorandil (100 µmol) can attenuate the level of apoptosis stimulated by high glucose significantly in H9C2 cardiomyocyte compared with the untreated group. The effect of nicorandil on apoptosis was blocked by 5‐HD, and it was accompanied with inhibition of the phosphorylation of PI3K, Akt, eNOS, and mTOR. After inhibition of PI3K/Akt pathway, the protective effect of nicorandil is restrained. These results verified that as a NO donor, nicorandil can also inhibit apoptosis in diabetic cardiomyopathy which is mediated by PI3K/Akt pathway.

Diabetic cardiomyopathy (DCM) is one of the leading causes of heart failure in patients with diabetes mellitus, with limited effective treatments. The cardioprotective effects of sodium‐glucose cotransporter 2(SGLT2) inhibitors have been supported by amounts of clinical trials, which largely fills the gap. However, the underlying mechanism still needs to be further explored, especially in terms of its protection against cardiac fibrosis, a crucial pathophysiological process during the development of DCM. Besides, endothelial‐to‐mesenchymal transition (EndMT) has been reported to play a pivotal role in fibroblast multiplication and cardiac fibrosis. This study aimed to evaluate the effect of SGLT2 inhibitor dapagliflozin (DAPA) on DCM especially for cardiac fibrosis and explore the underlying mechanism. In vivo, the model of type 2 diabetic rats was built with high‐fat feeding and streptozotocin injection. Untreated diabetic rats showed cardiac dysfunction, increased myocardial fibrosis and EndMT, which was attenuated after treatment with DAPA and metformin. In vitro, HUVECs and primary cardiac fibroblasts were treated with DAPA and exposed to high glucose (HG). HG‐induced EndMT in HUVECs and collagen secretion of fibroblasts were markedly inhibited by DAPA. Up‐regulation of TGF‐β/Smad signalling and activity inhibition of AMPKα were also reversed by DAPA treatment. Then, AMPKα siRNA and compound C abrogated the anti‐EndMT effects of DAPA in HUVECs. From above all, our study implied that DAPA can protect against DCM and myocardial fibrosis through suppressing fibroblast activation and EndMT via AMPKα‐mediated inhibition of TGF‐β/Smad signalling.

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Hypoxia-inducible factor 1α (HIF1α) promotes the malignant progression of glioblastoma under hypoxic conditions, leading to a poor prognosis for patients with glioblastoma; however, none of the therapies targeting HIF1α in glioblastoma have successfully eradicated the tumour. Therefore, we focused on the reason and found that treatments targeting HIF1α and HIF2α simultaneously increased tumour volume, but the combination of HIF1α/HIF2α-targeted therapies with temozolomide (TMZ) reduced tumourigenesis and significantly improved chemosensitization. Moreover, miR-210-3p induced HIF1α expression but inhibited HIF2α expression, suggesting that miR-210-3p regulates HIF1α/HIF2α expression. Epidermal growth factor (EGF) has been shown to upregulate HIF1α expression under hypoxic conditions. However, in the present study, in addition to the signalling pathways mentioned above, the upstream proteins HIF1α and HIF2α have been shown to induce EGF expression by binding to the sequences AGGCGTGG and GGGCGTGG. Briefly, in a hypoxic microenvironment the HIF1α/HIF2α-miR210-3p network promotes the malignant progression of glioblastoma through a positive feedback loop with EGF. Additionally, differentiated glioblastoma cells underwent dedifferentiation to produce glioma stem cells under hypoxic conditions, and simultaneous knockout of HIF1α and HIF2α inhibited cell cycle arrest but promoted proliferation with decreased stemness, promoting glioblastoma cell chemosensitization. In summary, both HIF1α and HIF2α regulate glioblastoma cell proliferation, dedifferentiation and chemoresistance through a specific pathway, which is important for glioblastoma treatments.

Serum amyloid A (SAA), a major acute-phase reactant, modulates angiogenesis in many diseases. Vascular endothelial growth factor receptor 2 (VEGFR2) is the primary angiogenic receptor for vascular endothelial growth factor (VEGF), but the possibility of an interaction between SAA and VEGFR2 has not yet been resolved. Here, we investigated if SAA stimulates the expression of VEGFR2 and promotes angiogenesis in vitro. Human umbilical vein endothelial cells (HUVECs) were stimulated with recombinant SAA (rSAA), and the messenger RNA (mRNA) and protein expression of VEGFR2 was detected by Western blot analysis and quantitative real-time PCR. Formyl peptide receptor-like 1 (FPRL1) agonist (WKYMVm) and antagonist (WRW(4)) and inhibitors of mitogen-activated protein kinases (MAPKs) were used to investigate the mechanism of regulation of VEGFR2.We show that SAA induces VEGFR2 expression in a time- and dose-dependent manner in HUVECs. In addition, SAA promotes tube formation in HUVECs. The effect of SAA on tube formation was shown to be the result of an increase in VEGFR2 expression, which was blocked by the multi-angiokinase receptor inhibitor BIBF1120. These activities of SAA appear to be mediated by FPRL1/MAPK signaling pathways, as they were mimicked by WKYMVm and abrogated by WRW(4) and inhibitors of MAPKs. These observations indicate that SAA induces VEGFR2 expression and promotes tube formation in HUVECs via the FPRL1/MAPK signaling pathway, thus providing a potential target for the control of angiogenesis.