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LncRNA LINK-A 重塑组织炎症微环境,促进肥胖

Yu Chen¹, Hui Chen¹, Ying Wang¹

¹MOE Laboratory of Biosystem Homeostasis and Protection, College of Life Sciences, Zhejiang University, Hangzhou, Zhejiang, 310058, China.

Advanced science (Weinheim, Baden-Wurttemberg, Germany)

|December 25, 2023

概括

高脂肪饮食肥胖症涉及炎症因素和破坏能量消耗. 针对 lncRNA LINK-A 显示出治疗肥胖和代谢综合征的前景.

科学领域:

分子生物学分子生物学
代谢性疾病研究研究
肥胖病原体的产生

背景情况:

高脂肪饮食 (HFD) 诱导的肥胖是代谢综合征的重要危险因素.
脂肪组织功能障碍是HFD诱导肥胖的一个关键因素,但潜在的机制尚未完全理解.
长非编码RNAs (lncRNAs) 越来越多地被认为是它们在代谢调节中的作用.

研究的目的:

为了确定HFD诱导的肥胖症中的关键分子参与者.
阐明 lncRNAs 影响能量消耗和代谢功能障碍的机制.
评估针对肥胖症中的特定 lncRNA 的治疗潜力.

主要方法:

基因查以确定与肥胖相关的 lncRNAs.
建立一个高脂肪饮食诱导的肥胖敲进 (KI) 鼠标模型.
分析炎症因子透,基因表达 (LINK-A,HB-EGF,HIF1α) 和代谢参数.
在体内测试针对LINK-A.的反感性寡核酸 (ASO).

主要成果:

鉴定出 lncRNA LINK-A 是 HFD 诱导的肥胖症中的一个关键分子.
通过一个自我放大的LINK-A/HB-EGF/HIF1α反循环,LINK-A促进炎症 (IL-1β,CXCL16).
这个轴破坏脂肪组织重塑和适应性热生成,导致肥胖和胰岛素抵抗.
在超重个体中,LINK-A表达与炎症标志物相关.
针对LINK-A的反感性寡核酸 (ASO) 有效地减少了HFD诱导的肥胖和代谢综合征.

结论:

通过重塑炎症组织微环境,LINK-A在调解HFD诱导的肥胖症方面发挥着至关重要的作用.
链接-A/HB-EGF/HIF1α轴是推动肥胖和胰岛素抵抗的关键途径.
将LINK-A与ASOs定位为对HFD诱导的肥胖和相关代谢障碍的潜在治疗策略.

关键词:

这就是HIF1α.这是一个LncRNARNA.有高脂肪的饮食.炎症性微环境是一种炎症微环境.肥胖肥胖肥胖肥胖肥胖肥胖肥胖肥胖治疗目标是治疗的目标.热生成是一种热生成.

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