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Rechargeable aqueous zinc–metal batteries (AZBs) are a promising complimentary technology to the existing lithium‐ion batteries and the re‐emerging lithium–metal batteries to satisfy the increasing demands on energy storage. Despite considerable progress achieved in the past years, the fundamental understanding of the solid‐electrolyte interphase (SEI) formation and how its composition influences the SEI properties are limited. This review highlights the functionalities of anion‐tuned SEI on the reversibility of zinc–metal anode, with a specific emphasis on new structural insights obtained through advanced characterizations and computational techniques. Recent efforts in terms of key variables that govern the interfacial behaviors to improve the long‐term stability of zinc anode, i.e., Coulombic efficiency, plating morphology, dendrite formation, and side‐reactions, are comprehensively reviewed. Lastly, the remaining challenges and future perspectives are presented, providing insights into the rational design of practical high‐performance AZBs. [ABSTRACT FROM AUTHOR]

Background: Diabetes mellitus (DM) and periodontitis are two prevalent diseases with mutual influence. Accumulation of advanced glycation end products (AGEs) in hyperglycemia may impair cell function and worsen periodontal conditions. N6-methyladenosine (m6A) is an important post-transcriptional modification in RNAs that regulates cell fate determinant and progression of diseases. However, whether m6A methylation participates in the process of periodontitis with diabetes is unclear. Thus, we aimed to investigate the effects of AGEs on bone marrow mesenchymal stem cells (BMSCs), elucidate the m6A modification mechanism in diabetes-associated periodontitis. Methods: Periodontitis with diabetes were established by high-fat diet/streptozotocin injection and silk ligation. M6A modifications in alveolar bone were demonstrated by RNA immunoprecipitation sequence. BMSCs treated with AGEs, fat mass and obesity associated (FTO) protein knockdown and sclerostin (SOST) interference were evaluated by quantitative polymerase chain reaction, western blot, immunofluorescence, alkaline phosphatase and Alizarin red S staining. Results: Diabetes damaged alveolar bone regeneration was validated in vivo. In vitro experiments showed AGEs inhibited BMSCs osteogenesis and influenced the FTO expression and m6A level in total RNA. FTO knockdown increased the m6A levels and reversed the AGE-induced inhibition of BMSCs differentiation. Mechanically, FTO regulated m6A modification on SOST transcripts, and AGEs affected the binding of FTO to SOST transcripts. FTO knockdown accelerated the degradation of SOST mRNA in presence of AGEs. Interference with SOST expression in AGE-treated BMSCs partially rescued the osteogenesis by activating Wnt Signaling. Conclusions: AGEs impaired BMSCs osteogenesis by regulating SOST in an m6A-dependent manner, presenting a promising method for bone regeneration treatment of periodontitis with diabetes. [ABSTRACT FROM AUTHOR]