Over the past two decades, the solid–electrolyte interphase (SEI) layer that forms on an electrode’s surface has been believed to be pivotal for stabilizing the electrode’s performance in lithium-ion batteries (LIBs). However, more and more researchers currently are realizing that the metal-ion solvation structure (e.g., Li+) in electrolytes and the derived interfacial model (i.e., the desolvation process) can affect the electrode’s performance significantly. Thus, herein we summarize recent research focused on how to discover the importance of an electrolyte’s solvation structure, develop a quantitative model to describe the solvation structure, construct an interfacial model to understand the electrode’s performance, and apply these theories to the design of electrolytes. We provide a timely review on the scientific relationship between the molecular interactions of metal ions, anions, and solvents in the interfacial model and the electrode’s performance, of which the viewpoint differs from the SEI interpretations before. These discoveries may herald a new, post-SEI era due to their significance for guiding the design of LIBs and their performance improvement, as well as developing other metal-ion batteries and beyond.

The blood-brain barrier (BBB) establishes a protective interface between the central neuronal system and peripheral blood circulation and is crucial for homeostasis of the CNS. BBB formation starts when the endothelial cells (ECs) invade the CNS and pericytes are recruited to the nascent vessels during embryogenesis. Despite the essential function of pericyte-EC interaction during BBB development, the molecular mechanisms coordinating the pericyte-EC behavior and communication remain incompletely understood. Here, we report a single cell receptor, CD146, that presents dynamic expression patterns in the cerebrovasculature at the stages of BBB induction and maturation, coordinates the interplay of ECs and pericytes, and orchestrates BBB development spatiotemporally. In mouse brain, CD146 is first expressed in the cerebrovascular ECs of immature capillaries without pericyte coverage; with increased coverage of pericytes, CD146 could only be detected in pericytes, but not in cerebrovascular ECs. Specific deletion of Cd146 in mice ECs resulted in reduced brain endothelial claudin-5 expression and BBB breakdown. By analyzing mice with specific deletion of Cd146 in pericytes, which have defects in pericyte coverage and BBB integrity, we demonstrate that CD146 functions as a coreceptor of PDGF receptor-β to mediate pericyte recruitment to cerebrovascular ECs. Moreover, we found that the attached pericytes in turn downregulate endothelial CD146 by secreting TGF-β1 to promote further BBB maturation. These results reveal that the dynamic expression of CD146 controls the behavior of ECs and pericytes, thereby coordinating the formation of a mature and stable BBB.lood-brain barrier (BBB) development is a sequential and well-orchestrated process that commences when brain endothelial cells (ECs; BECs) invade the embryonic neuroectoderm from the surrounding vascular plexus and induce BBB properties by establishing paracellular tight junctions (TJs) (1). Endothelial TJs are formed by a complex of transmembrane proteins, including claudins and occludin, as well as cytoplasmic adaptors such as zonula occludens protein 1 (ZO-1), thus creating a highresistance paracellular barrier to molecules and ions (2). Compelling evidence shows that claudin-5 plays a key role in the induction of BBB properties, and specific loss of claudin-5 in mice results in a more leaky BBB (3-5). Following the establishment of the TJs, the BECs of nascent vessels recruit pericytes to the endothelial walls, which improve the barrier function of BECs by stabilizing TJs and decreasing transcytosis, and are crucial for maturation of the BBB (6). Importantly, pericytes suppress the expression of leukocyte adhesion molecules (LAMs) in BECs to reduce the invasion of immune cells into the CNS, therefore regulating CNS immune surveillance, a critical feature of the mature BBB (6, 7). Thus, as a dynamic interface with a range of interrelated functions, the BBB results from extremely effective TJs, pericyte recruitment, and regulation of leukocyte extravasation, there...