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The strategy of molecular engineering has been employed to build the structure–property–activity relationship for covalent organic frameworks (COFs) with efficient photocatalytic water splitting for hydrogen production. However, previous reports focus on the impact of molecular design on COFs' physicochemical properties, the crystallinity differences are usually ignored and related studies remain rare. Herein, we describe the preparation of a series of structurally related COFs with similar chemical compositions but have different numbers of nitrogen (N) atoms in the central aromatic ring via an efficient crystallization strategy using of 2,4,6-triformyl resorcinol (TFR). On one hand, the introduction of N atoms reduces π-π stacking interaction during the formation of framework, leading to a decrease in crystallinity. On the other hand, it contributes to enhancing the photocatalytic performance of the materials by varying the electronic structures. Consequently, our results revealed that the photocatalytic hydrogen evolution (PHE) rate is 61.22 mmol g−1 h−1 for COF-905-1N, significantly higher than COF-905-3N (40.60 mmol g−1 h−1) and COF-905 (26.23 mmol g−1 h−1). This study not only provide fundamental insights into formation mechanism of COFs, but also provide a practical approach to enhance COF-based photocatalytic performance. We synthesized three COFs (COF-905, COF-905-1N, and COF-905-3N) with varying number of nitrogen atoms, resulting in different crystallinity via molecular engineering. COF-905-1N shows the highest photocatalytic hydrogen production performance with a rate up to 61.22 mmol g−1 h−1. The water-drainage experiments also suggest the potential of COF-905-1N in the practical applications for photocatalytic hydrogen evolution. [Display omitted] • Three structurally related COFs were constructed via an efficient crystallization strategy based on the use of TFR. • The crystallinity of the resultant COFs decreases as the number of N atoms in the central benzene ring increases. • The π-π stacking between the intermediate macrocycles becomes less favorable, leading to incompact stacking of 2D layers. • COF-905-1N exhibits superior PHE performance under the combined influence of nitrogen content and crystallinity. [ABSTRACT FROM AUTHOR]

• FGFR2 was upregulated in psoriatic lesion tissues. • Inhibition of FGFR2 significantly inhibited the keratinocyte proliferation and migration. • miR-124-3p was downregulated within psoriasis and could directly target FGFR2. • miR124-3p/FGFR2 axis inhibit keratinocyte proliferation, migration, and improve the inflammatory microenvironment. Keratinocyte hyperproliferation has been regarded as a central event in psoriasis pathogenesis. Investigating the mechanisms of keratinocyte hyperproliferation might provide novel strategies for psoriasis treatment. we demonstrated that fibroblast growth factor receptor 2 (FGFR2) expression was abnormally upregulated within psoriatic lesion tissues and HaCaT cells under rIL-22 stimulation. FGFR2 silence within HaCaT cells under rIL-22 stimulation significantly inhibited the capacity of cells to proliferate and to migrate, reduced IL-17A and TNFα mRNA expression, and decreased the protein levels of FGFR2, keratin 6, keratin 16, MMP1, MMP9, p-PI3K, p-AKT and p-ERK. In contrast to FGFR2, the expression of miR-124-3p showed to be remarkably downregulated within psoriasis lesion tissue samples and rIL-22-stimulated HaCaT cells. miR-124-3p inhibited the expression of FGFR2 via direct binding to its 3'UTR. Within HaCaT cells under rIL-22 stimulation, the overexpression of miR-124-3p also suppressed the capacity of cells to proliferate and to migrate, reduced IL-17A and TNFα mRNA expression, and decreased the protein levels of FGFR2, keratin 6, keratin 16, MMP1, MMP9 and p-PI3K, p-AKT and p-ERK. More importantly, when co-transfected to HaCaT cells, FGFR2-overexpressing vector significantly attenuated the effects of miR-124-3p mimics on HaCaT cells. In conclusion, we demonstrated an miR124-3p/FGFR2 axis that might inhibit human keratinocyte proliferation, migration, and improve the inflammatory microenvironment in psoriasis. miR124-3p/FGFR2 axis could be an underlying target for psoriasis therapy, which requires further in vivo and clinical investigation. [ABSTRACT FROM AUTHOR]