In recent years, Pb-free CsSnI3 perovskite materials with excellent photoelectric properties as well as low toxicity are attracting much attention in photoelectric devices. However, deep level defects in CsSnI3, such as high density of tin vacancies, structural deformation of SnI6− octahedra and oxidation of Sn2+ states, are the major challenge to achieve high-performance CsSnI3-based photoelectric devices with good stability. In this work, defect passivation method is adopted to solve the above issues, and the ultra-stable and high-performance CsSnI3 nanowires (NWs) photodetectors (PDs) are fabricated via incorporating 1-butyl-2,3-dimethylimidazolium chloride salt (BMIMCl) into perovskites. Through materials analysis and theoretical calculations, BMIM+ ions can effectively passivate the Sn-related defects and reduce the dark current of CsSnI3 NW PDs. To further reduce the dark current of the devices, the polymethyl methacrylate is introduced, and finally, the dual passivated CsSnI3 NWPDs show ultra-high performance with an ultra-low dark current of 2 × 10–11 A, a responsivity of up to 0.237 A W−1, a high detectivity of 1.18 × 1012 Jones and a linear dynamic range of 180 dB. Furthermore, the unpackaged devices exhibit ultra-high stability in device performance after 60 days of storage in air (25 °C, 50% humidity), with the device performance remaining above 90%.

Cost-effective treatment strategies for liver fibrosis or cirrhosis are limited. Many clinical trials of stem cells for liver disease shown that stem cells might be a potential therapeutic approach. This review will summarize the published clinical trials of stem cells for the treatment of liver fibrosis/cirrhosis and provide the latest overview of various cell sources, cell doses, and delivery methods. We also describe the limitations and strengths of various stem cells in clinical applications. Furthermore, to clarify how stem cells play a therapeutic role in liver fibrosis, we discuss the molecular mechanisms of stem cells for treatment of liver fibrosis, including liver regeneration, immunoregulation, resistance to injury, myofibroblast repression, and extracellular matrix degradation. We provide a perspective for the prospects of future clinical implementation of stem cells.

Background Effective therapeutics to stop or reverse liver fibrosis have not emerged, because these potential agents cannot specifically target activated hepatic stellate cells (aHSCs) or are frequently toxic to parenchymal cells. Human umbilical cord mesenchymal stem cell (Huc-MSC)-derived exosomes show promise in nanomedicine for the treatment of liver fibrosis. However, systemic injection showed that unmodified exosomes were mainly taken up by the mononuclear phagocyte system. The discovery of ligands that selectively bind to a specific target plays a crucial role in clinically relevant diagnostics and therapeutics. Herein, we aimed to identify the targeting peptide of aHSCs by screening a phage-displayed peptide library, and modify Huc-MSC-derived exosomes with the targeting peptide. Results In this study, we screened a phage-displayed peptide library by biopanning for peptides preferentially bound to HSC-T6 cells. The identified peptide, HSTP1, also exhibited better targeting ability to aHSCs in pathological sections of fibrotic liver tissues. Then, HSTP1 was fused with exosomal enriched membrane protein (Lamp2b) and was displayed on the surface of exosomes through genetic engineering technology. The engineered exosomes (HSTP1-Exos) could be more efficiently internalized by HSC-T6 cells and outperformed both unmodified exosomes (Blank-Exos) and Lamp2b protein overexpressed exosomes (Lamp2b + Exos) in enhancing the ability of exosomes to promote HSC-T6 reversion to a quiescent phenotype. In vivo results showed HSTP1-Exos could specifically target to the aHSC region after intravenous administration, as demonstrated by coimmunofluorescence with the typical aHSCs marker α-SMA, and enhance the therapeutic effect on liver fibrosis. Conclusion These results suggest that HSTP1 is a reliable targeting peptide that can specifically bind to aHSCs and that HSTP1-modified exosomes realize the precise treatment for aHSCs in complex liver tissue. We provide a novel strategy for clinical liver fibrosis therapy. Graphical Abstract

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