重编程
银屑病
新陈代谢
糖酵解
下调和上调
碳水化合物代谢
葡萄糖摄取
内科学
代谢综合征
PI3K/AKT/mTOR通路
生物
癌症研究
内分泌学
医学
细胞生物学
生物化学
糖尿病
免疫学
信号转导
胰岛素
细胞
基因
作者
Liang Yan,Wen‐qiu Wang,Yuxin Qiu,Chongli Yu,Rui Wang,Chengxin Li
标识
DOI:10.1016/j.intimp.2024.112704
摘要
The mechanism linking psoriasis to metabolic syndrome (MetS) remains poorly understood. Recent reports indicate upregulation of glycolysis-related proteins in psoriatic keratinocytes (KCs). However, the role of glucose metabolism reprogramming in psoriatic KCs, psoriasis, and psoriasis with MetS remains unclear. In this study, we confirmed glucose metabolism reprogramming in psoriatic KCs by examining glycolysis-related genes, proteins, and metabolites. We found that inhibiting glucose metabolism reprogramming in psoriasiform KCs led to improvements in psoriasiform features. Notably, we observed enhanced glucose metabolism reprogramming in KCs within psoriatic skin lesions of patients with MetS. In vitro, high-glucose and high-fat culture intensified glucose metabolism reprogramming in psoriasiform KCs partially via the AKT/mTOR pathway. These findings highlight a strong link between the glycolytic switch and KC function and suggest that glucose metabolism reprogramming in KCs contributes to heightened psoriatic inflammation in MetS.
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