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通过通过激活GCH1来抑制内皮细胞铁亡,CTRP13可以减轻动脉样硬化

Jie Du¹, Xinxin Zhu², Youqi Zhang²

¹Harbin Medical University, Harbin 150001, PR China; Department of Cardiology, The Fourth Affiliated Hospital of Harbin Medical University, Harbin 150001, PR China; Key Laboratory of Myocardial Ischemia, Ministry of Education, Harbin 150001, PR China.

International immunopharmacology

|November 14, 2024

概括

与C1q/TNF相关的蛋白13 (CTRP13) 通过激活GCH1/BH4通路来保护内皮细胞免受铁. 这一发现揭示了CTRP13的存在.

科学领域:

心血管生物学心血管生物学
细胞的新陈代谢
分子医学是分子医学.

背景情况:

与C1q/TNF相关的蛋白13 (CTRP13) 是一种分泌的阿迪波金,与心血管疾病有关.
目前尚不清楚CTRP13在内皮细胞铁亡中的作用及其潜在机制.

研究的目的:

为了研究CTRP13对内皮功能障碍和高脂质诱导动脉样硬化中的铁.
阐明CTRP13发挥其保护作用的分子机制.

主要方法:

在体内研究使用高脂肪食的ApoE-/-小鼠与CTRP13基因过度表达.
在体外实验中,使用用CTRP13.3治疗的ox-LDL诱导的小鼠大动脉内皮细胞 (MAEC) 进行了实验.
评估动脉样硬化斑块特征,细胞活力,脂质过氧化,铁沉积,线粒体功能和关键蛋白质表达 (GPX4,ACSL4).

主要成果:

在内皮细胞中,CTRP13抑制了铁亡,由增加的GPX4和减少的ACSL4表达体现出来.
GCH1/BH4信号通路的CTRP13激活对其保护作用至关重要.
沉默GCH1或抑制BH4逆转了CTRP13的保护作用,恶化了内皮功能障碍.

结论:

通过激活GCH1/BH4通路,CTRP13保护内皮细胞免受铁和功能障碍.
CTRP13减轻了线粒体的氧化应激,并抑制了动脉样硬化的进展.
CTRP13代表了涉及内皮功能障碍的心血管疾病的潜在治疗标.

关键词:

动脉样硬化是一种动脉样硬化.BH4 BH4 BH4 BH4 BH4 BH4 BH4 BH4 BH4 BH4 BH4 在CTRP13中使用.内皮细胞是内皮细胞.铁化是铁化的一种.在 GCH1 中.

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