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抑制TLR4通过调节FTO介导的m6A修饰来预防糖尿病骨损失

Ximei Shen¹, Chao Lan¹, Youfen Lin¹

¹Department of Endocrinology, The First Affiliated Hospital, Fujian Medical University, Fuzhou 350005, China; Department of Endocrinology, National Regional Medical Center, Binhai Campus of the First Affiliated Hospital, Fujian Medical University, Fuzhou 350212, China; Clinical Research Center for Metabolic Diseases of Fujian Province, The First Affiliated Hospital, Fujian Medical University, Fuzhou 350005, China; Fujian Key Laboratory of Glycolipid and Bone Mineral Metabolism, The First Affiliated Hospital, Fujian Medical University, Fuzhou 350005, China; Diabetes Research Institute of Fujian Province, The First Affiliated Hospital, Fujian Medical University, Fuzhou 350005, China; Metabolic Diseases Research Institute, The First Affiliated Hospital, Fujian Medical University, Fuzhou 350005, China.

International immunopharmacology

|July 6, 2023

概括

托尔类受体-4 (TLR4) 抑制通过调节N6-甲基氨酸 (m⁶A) 修饰来防止糖尿病骨损失. 这种表观遗传变化影响了糖尿病大鼠的骨质细胞分化和骨矿物质密度.

科学领域:

分子生物学分子生物学
内分泌学在内分泌学.
骨的新陈代谢骨的新陈代谢

背景情况:

糖尿病骨质疏松症是一个越来越令人担忧的疾病,其发展与托尔类受体-4 (TLR4) 有关.
对于TLR4在糖尿病患者骨代谢中的作用以及表观遗传修饰的贡献的确切机制尚不清楚.
N6-甲基氨酸 (m6A) 是一种流行的mRNA表观遗传修饰,可能与骨质疏松症风险有关.

研究的目的:

为了研究TLR4是否调节糖尿病大鼠骨组织的m6A修饰.
阐明TLR4-介导的m⁶A变化在糖尿病骨质损失的发病过程中的作用.

主要方法:

N6-甲基氨酸测序 (m6A-seq) 在野生型和TLR4敲击型糖尿病大鼠的股骨样本上进行.
基因本体学丰富分析被用来识别差异修饰的基因和相关的生物过程.
定量逆转录PCR (qRT-PCR) 评估了m6A甲基转移酶和脱甲基酶的表达.
在实验室中使用骨质细胞模型来确认TLR4介导的效应.

主要成果:

糖尿病大鼠的TLR4淘汰会防止体重减轻,并显著增加骨矿物质密度 (BMD).
m6A-seq在TLR4-淘汰赛大鼠中与骨质细胞分化相关的基因中发现了差异性m6A修饰.
m6A脱甲基酶,脂肪质量和与肥胖相关的蛋白质 (FTO) 在TLR4失败的糖尿病大鼠中显示出减少表达.
证实TLR4介导的骨质细胞分化是由通过FTO抑制诱导的甘油脂毒性引起的.

结论:

在糖尿病期间,TLR4在调节m6骨组织内的修饰中发挥着关键作用.
抑制TLR4可以作为预防糖尿病骨损失的治疗策略.
通过FTO介导的m6A通路是TLR4影响糖尿病骨代谢的关键机制.

关键词:

骨的新陈代谢骨的新陈代谢糖尿病糖尿病糖尿病在 FTO FTO FTO.在TLR4中,m6A 一个很好的.

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