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巨噬细胞中的(某种因素)促进了对肥胖的介导敏感性。 (注:原句不太完整,翻译出来的中文表述可能不太通顺,最好能提供更完整准确的原文。)

in macrophages promotes mediated sensitivity to obesity.

作者信息

Wang Rong, Gao Yunhuan, Wang Ya, Zhang Yuan, Yang Rongcun

机构信息

Department of Immunology, Nankai University School of Medicine, Nankai University, Tianjin, China.

Translational Medicine Institute, Affiliated Tianjin Union Medical Center of Nankai University, Tianjin, China.

出版信息

Front Immunol. 2025 Apr 28;16:1574507. doi: 10.3389/fimmu.2025.1574507. eCollection 2025.

Abstract

Lipopolysaccharide (LPS, endotoxin) -mediated signaling of caspase-4 (human) and -11 (rodent) can induce the maturation of inflammatory cytokine IL-1β and cell pyroptosis, which is associated with the pathophysiology of many diseases such as obesity. However, the process by which LPS induces inflammation through caspase 4/11 is not fully understood. We found here that plays a key role in LPS-mediated maturation of inflammatory cytokine IL-1β and pyroptosis of macrophages. Mechanistic ally, the binding of caspase 4/11 to LPS requires to cause activation of the caspase 4/11 complex, which ultimately caused inflammation to promote sensitivity to high fat diet (HFD) -mediated obesity. Notably, expression can be up-regulated by LPS. This lncRNA29 is highly conserved between humans and mice. Taken together, these results suggest that determines the occurrence and progression of LPS-related diseases such as obesity.

摘要

脂多糖(LPS,内毒素)介导的半胱天冬酶-4(人类)和-11(啮齿动物)信号传导可诱导炎性细胞因子IL-1β成熟和细胞焦亡,这与许多疾病如肥胖症的病理生理学相关。然而,LPS通过半胱天冬酶4/11诱导炎症的过程尚未完全了解。我们在此发现, 在LPS介导的炎性细胞因子IL-1β成熟和巨噬细胞焦亡中起关键作用。机制上,半胱天冬酶4/11与LPS的结合需要 来激活半胱天冬酶4/11复合物,最终导致炎症,促进对高脂饮食(HFD)介导的肥胖症的易感性。值得注意的是, 的表达可被LPS上调。这种长链非编码RNA29在人类和小鼠之间高度保守。综上所述,这些结果表明, 决定了肥胖症等LPS相关疾病的发生和发展。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f81d/12066258/ba65e330bcab/fimmu-16-1574507-g001.jpg

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