Inhibition of DYRK1B BY C81 impedes inflammatory processes in leukocytes by reducing STAT3 activity.

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Tác giả: Lena Berger, Franz Bracher, Luisa D Burgers, Sarah Ciurus, Mohammed A F Elewa, Dominik C Fuhrmann, Robert Fürst, Gerd Geisslinger, Robert Gurke, Mandy Hector, Stefan Knapp, Thomas Langmann, Rolf Marschalek, Megan A Palmer, Martin P Schwalm, Dominique Thomas, Andreas Weigert, Anne Wolf, Thomas J Zech

Ngôn ngữ: eng

Ký hiệu phân loại: 324.54 Nominating by primaries

Thông tin xuất bản: Switzerland : Cellular and molecular life sciences : CMLS , 2025

Mô tả vật lý:

Bộ sưu tập: NCBI

ID: 551471

Chronic inflammatory diseases are a significant global burden and are associated with dysregulated resolution of inflammation. Therefore, promoting the process of resolution is a promising therapeutic approach. This study presents the potent anti-inflammatory and pro-resolving effects of a natural product-derived compound called C81. Administration of C81 in a therapeutic window resolved inflammation in the murine imiquimod-induced psoriasis model, and reduced microglial infiltration in a laser-induced choroidal neovascularisation model. Investigations into the underlying mechanisms of C81 identified the DYRK1B/STAT3 axis as a new regulator of inflammatory processes in leukocytes. The inhibition of DYRK1B by C81 resulted in attenuated STAT3 phosphorylation. The depletion of STAT3-regulated gene expression led to the inhibition of leukocyte adhesion and migration due to reduced integrin activation, and in addition to the inhibition of the release of pro-inflammatory mediators such as cytokines and eicosanoids. Importantly, the pro-resolving effects of C81 included the cell type-specific induction of apoptosis in neutrophils and a subsequent increase in efferocytosis. In conclusion, we report the DYRK1B/STAT3 axis as a novel and promising therapeutic target for activating the resolution of inflammation.
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