Recent progresses and challenges in aqueous lithium-air batteries relating to the solid electrolyte separator: A mini-review.

The lithium-air (Li-air) battery utilizes infinite oxygen in the air to store or release energy through a semi-open cathode structure and bears an ultra-high theoretical energy density of more than 1,000 Wh/kg. Therefore, it has been denoted as the candidate for next-generation energy storage in versatile fields such as electric vehicles, telecommunications, and special power supply. Among all types of Li-air batteries, an aqueous Li-air battery bears the advantages of a high theoretical energy density of more than 1,700 Wh/kg and does not have the critical pure oxygen atmosphere issues in a non-aqueous lithium-air battery system, which is more promising for the actual application. To date, great achievements have been made in materials' design and cell configurations, but critical challenges still remain in the field of the solid electrolyte separator, its related lithium stripping/plating at the lithium anode, and catholyte design. In this mini-review, we summarized recent progress related to the solid electrolyte in aqueous Li-air batteries focusing on both material and battery device development. Moreover, we proposed a discussion and unique outlook on improving solid electrolyte compatibility and battery performance, thus designing an aqueous Li-air battery with higher energy density and better cycle performance in the future.

Downregulation of a mitochondrial micropeptide, MPM, promotes hepatoma metastasis by enhancing mitochondrial complex I activity.

We and others have shown that MPM (micropeptide in mitochondria) regulates myogenic differentiation and muscle development. However, the roles of MPM in cancer development remain unknown. Here we revealed that MPM was downregulated significantly in human hepatocellular carcinoma (HCC) tissues and its decrease was associated with increased metastasis potential and HCC recurrence. Gain- and loss-of-function investigations disclosed that in vitro migration/invasion and in vivo liver/lung metastasis of hepatoma cells were repressed by restoring MPM expression and increased by silencing MPM. Mechanism investigations revealed that MPM interacted with NDUFA7. Mitochondrial complex I activity was inhibited by overexpressing MPM and enhanced by siMPM, and this effect of siMPM was attenuated by knocking down NDUFA7. The NAD+/NADH ratio, which was regulated by complex I, was reduced by MPM but increased by siMPM. Treatment with the NAD+ precursor nicotinamide abrogated the inhibitory effect of MPM on hepatoma cell migration. Further investigations showed that miR-17-5p bound to MPM and inhibited MPM expression. miR-17-5p upregulation was associated with MPM downregulation in HCC tissues. These findings indicate that a decrease in MPM expression may promote hepatoma metastasis by increasing mitochondrial complex I activity and the NAD+/NADH ratio.