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急性细胞因子治疗可刺激人角质细胞的葡萄糖摄取和糖酵解。

Acute cytokine treatment stimulates glucose uptake and glycolysis in human keratinocytes.

机构信息

Pediatric Translational Research Branch, National Institute of Arthritis and Musculoskeletal and Skin Diseases, National Institutes of Health, Bethesda, MD, USA.

Department of Experimental Medical Science, Lund University, Sweden.

出版信息

Cytokine. 2023 Jan;161:156057. doi: 10.1016/j.cyto.2022.156057. Epub 2022 Oct 5.

Abstract

During inflammation, cellular glucose uptake and glycolysis are upregulated to meet an increased energy demand. For example, keratinocyte glycolysis is essential for progression of psoriasis. Therefore, understanding the regulation of glucose metabolism in keratinocytes is of importance. Here, we show that the pro-inflammatory cytokines IFNγ and TNF together rapidly induce glucose uptake, glycolysis, and glycolytic capacity in cultured keratinocytes. Furthermore, we found that acute IFNγ and TNF stimulation induces glucose transporter 4 (GLUT4) translocation to the plasma membrane and engages AMPK-dependent intracellular signaling. Together, these findings suggest acute cytokine-induced glucose metabolism in keratinocytes could contribute to inflammation in psoriatic disease, and that GLUT4 is involved in these processes.

摘要

在炎症过程中,细胞葡萄糖摄取和糖酵解会被上调以满足增加的能量需求。例如,角质形成细胞的糖酵解对于银屑病的进展是必不可少的。因此,了解角质形成细胞中葡萄糖代谢的调节具有重要意义。在这里,我们表明促炎细胞因子 IFNγ 和 TNF 一起可迅速诱导培养的角质形成细胞中葡萄糖摄取、糖酵解和糖酵解能力。此外,我们发现急性 IFNγ 和 TNF 刺激诱导葡萄糖转运蛋白 4 (GLUT4)易位到质膜,并参与 AMPK 依赖性细胞内信号转导。总之,这些发现表明角质形成细胞中急性细胞因子诱导的葡萄糖代谢可能有助于银屑病疾病中的炎症,并且 GLUT4 参与这些过程。

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