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MXenes, a class of two-dimensional transition metal carbides, nitrides, and carbonitrides, have garnered significant attention due to their remarkable potential for energy storage, electrocatalysis, and gas separation applications. The fabrication processes of MXene involve building up the MXene structure from constituent elements and the selective elimination of M-A bonds from the precursor MAX. However, considerable efforts are still required to design and develop efficient MXene-based technologies. This review article aims to briefly analyse the synthesis methods employed for MXene production, ranging from direct synthesis and conventional chemical wet etching approach to the more recent molten salt etching technique. The review highlights the advancements made in achieving precise control over the terminal groups, which is paramount for tailoring the properties of MXenes for specific applications. Furthermore, the potential of MXene-based materials for carbon capture applications, particularly in developing advanced adsorbents, is emphasized. The in-depth examination of MXene synthesis techniques and their implications for carbon capture applications provides a solid foundation for developing and optimizing these promising materials.
RESUMO
BACKGROUND: Circular RNAs (circRNAs) can play a critical role in rheumatoid arthritis (RA) pathogenesis by involving gene regulation by competing for shared microRNAs (miRNAs), a family of small noncoding RNAs. MiR-130a-3p is a disease-related miRNA and Kruppel-like factor 9 (KLF9) is a zinc finger transcription factor, which are involved in RA pathogenesis. Here, we identified the action of circRNA circ_0130438 in regulating fibroblast-like synoviocytes (FLSs) stimulated by tumor necrosis factor α (TNF-α). METHODS: The direct relationship between miR-130a-3p and circRNA circ_0130438 or KLF9 was predicted by bioinformatics analysis and examined by a dual-luciferase reporter or RNA immunoprecipitation (RIP) assay. CircRNA circ_0130438, miR-130a-3p and KLF9 factor expression levels were gauged by a quantitative real-time PCR (qRT-PCR) or a western blot method. Cell proliferation ability was analyzed by a 5-Ethynyl-2'-Deoxyuridine (EdU) staining assay. The transwell assay was used to evaluate cell migration and invasion capacities. The production levels of interleukin-1ß (IL)-1ß, IL-6 and IL-8 were assessed by enzyme-linked immunosorbent assay (ELISA). RESULTS: The level of circRNA circ_0130438 was reduced in RA tissues (P = 0.0001) and FLSs isolated from RA tissues (P = 0.0001) compared with corresponding normal controls. Exposure of human fibroblast-like MH7A synoviocytes to TNF-α suppressed circRNA circ_0130438 expression (P < 0.0001). In contrast, the elevated expression of circRNA circ_0130438 suppressed the TNF-α-induced proliferation (P = 0.0047) and migration (P = 0.0023) of MH7A cells, as well as their pro-inflammatory cytokines (IL-1ß, IL-6 and IL-8) production (P < 0.0001, P < 0.0001 and P < 0.0001). The circRNA circ_0130438 contained a miR-130a-3p binding site. Furthermore, the increase of miR-130-3p in TNF-α-stimulated MH7A cells reversed the effects of circRNA circ_0130438 elevation on cell proliferation (P = 0.0006), migration (P = 0.0406) and pro-inflammatory cytokines (IL-1ß, IL-6 and IL-8) production (P = 0.0036, P < 0.0001 and P = 0.0004), indicating that miR-130a-3p was a functional mediator of circRNA circ_0130438 regulation. We also documented that KLF9 was a direct target and downstream effector of miR-130a-3p. Importantly, circRNA circ_0130438 enhanced KLF9 expression (P < 0.0001) in TNF-α-stimulated MH7A cells by functioning as a competing endogenous RNA (ceRNA) for miR-130a-3p (P = 0.0004). CONCLUSION: Our findings demonstrate that the elevated expression of circRNA circ_0130438 suppresses TNF-α-induced migration, proliferation and pro-inflammatory cytokines (IL-1ß, IL-6 and IL-8) production of human MH7A cells by enhancing KLF9 expression by operating as a ceRNA for miR-130a-3p.