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Aims: The N6-methyladenosine (m 6 A) modification plays an important role in various biological processes, but its role in atherosclerosis remains unknown. The aim of this study was to investigate the role and mechanism of m 6 A modification in endothelial cell inflammation and its influence on atherosclerosis development. Methods: We constructed a stable TNF-α-induced endothelial cell inflammation model and assessed the changes in the expression of m 6 A modification-related proteins to identify the major factors involved in this process. The m 6 A-modified mRNAs were identified by methylated RNA immunoprecipitation (RIP) sequencing and forkhead box O1 (FOXO1) was selected as a potential target. Through cytological experiments, we verified whether methyltransferase-like 14 (METTL14) regulates FOXO1 expression by regulating m 6 A-dependent mRNA and protein interaction. The effect of METTL14 on atherosclerosis development in vivo was verified using METTL14 knockout mice. Results: These findings confirmed that METTL14 plays major roles in TNF-α-induced endothelial cell inflammation. During endothelial inflammation, m 6 A modification of FOXO1, an important transcription factor, was remarkably increased. Moreover, METTL14 knockdown significantly decreased TNF-α-induced FOXO1 expression. RIP assay confirmed that METTL14 directly binds to FOXO1 mRNA, increases its m 6 A modification, and enhances its translation through subsequent YTH N6-methyladenosine RNA binding protein 1 recognition. Furthermore, METTL14 was shown to interact with FOXO1 and act directly on the promoter regions of VCAM-1 and ICAM-1 to promote their transcription, thus mediating endothelial cell inflammatory response. In vivo experiments showed that METTL14 gene knockout significantly reduced the development of atherosclerotic plaques. Conclusion: METTL14 promotes FOXO1 expression by enhancing its m 6 A modification and inducing endothelial cell inflammatory response as well as atherosclerotic plaque formation. Decreased expression of METTL14 can inhibit endothelial inflammation and atherosclerosis development. Therefore, METTL14 may serve as a potential target for the clinical treatment of atherosclerosis.

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Graphite has been widely used as a negative electrode in LIBs, where the reversible intercalation of Li + into the graphite layers forms binary compounds (b-GICs) with the stoichiometric composition of LiC 6. [9-11] However, an early attempt to use graphite as an anode for SIBs was unsuccessful because capacities less than 35 mAh g −1 were achieved. [12-14] This may be mistakenly attributed to the higher radius of Na + (0.102 nm) as compared with that of Li + (0.076 nm). [15-19] However, the instability of the Na-GICs resulted in poor sodium storage in graphite. [20-22] Owing to the diglyme-graphene vdW interaction, [23] the co-intercalation of the solvated Na ions effectively formed stable ternary graphite intercalation compounds (t-GICs) with the common formula Na(solv) y C 20 (y = 1 or more likely 2). [24,25] The formation of t-GICs at approximately 0.5-0.6 V (vs Na + /Na) is accompanied by a pronounced volume expansion in the ether-based electrolyte. The average electrode thickness reportedly increases by approximately 100 µm (50 µm in the pristine electrode) after sodiation. Furthermore, the original value is 3.4 Å which increase to the value within the range of 11.3 to 11.9 Å that indicates a 300-340% volume expansion. [26,27] The huge volume changes resulted in the formation of an unstable interphase that causes a rapid decay in the capacity of the anode material. This is typified by the silicon-based materials in LIBs. [28,29] The solid electrolyte interphase (SEI) that is formed during the initial cycle hinders Considerable efforts have been exerted to understand the formation and properties of the solid electrolyte interphase (SEI) in sodium ion batteries. However, the puzzling existence and role of SEI behind the huge volume changes of the graphite electrodes need to be answered. Herein, the reason of how ether-derived SEI maintains excellent reversibility despite the huge volume changes during cycling is unraveled. Theoretical simulations and Fourier-transform infrared spectroscopy demonstrate the formation mechanism of an SEI between the graphite anode and electrolyte. Furthermore, the high mechanical tolerance of the ether-derived SEI is confirmed in atomic force microscopy. A depth profile of X-ray photoelectron spectroscopy points to a multilayer structure of the ether-derived SEI. The outer layer comprises organics (sodium alkoxide), while the inorganics (Na 2 CO 3 , NaF) in interior region are mixed with some organics. Notably, the presence of organics ensures the adaptability of the SEI to the volume expansion of graphite during cycling, and the concentrated distribution of inorganics improves the Young's modulus (resistance to deformation). Therefore, the graphite anode exhibits high cycle stability (96.6% capacity retention ratio at 1 A g-1 over 860 cycles) and efficiency (≈99.5%).