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由RCN1下调驱动的内质网膜应激会损害内皮功能和糖尿病足的愈合

Zhiyan Weng¹, Xiaoyan Ren¹, Wanxin Lin¹

¹Department of Endocrinology, the First Affiliated Hospital of Fujian Medical University, 20 Cha Zhong Road, Fuzhou, 350005, China.

Cellular and molecular life sciences : CMLS

|August 25, 2025

概括

通过增加内质网膜 (ER) 应激和内皮功能障碍,红细胞1 (RCN1) 缺乏会使糖尿病足 (DFU) 恶化. 在糖尿病模型中恢复RCN1水平有助于愈和血管生成.

科学领域:

内分泌学
血管生物学
细胞生物学

背景情况:

糖尿病足是主要的发病和死亡原因.
内皮功能障碍和内质网膜 (ER) 压力是不治愈的DFU的关键因素.
连接ER应激与内皮功能障碍的确切机制尚不清楚.

研究的目的:

在糖尿病足发病过程中研究Reticulocalbin 1 (RCN1) 的作用.
阐明RCN1影响内皮细胞功能和ER应激的机制.
评估RCN1作为改善DFU愈合的潜在治疗点.

主要方法:

用于评估愈,血管生成和RCN1表达的糖尿病小鼠模型.
对暴露于糖脂毒性的人类静脉内皮细胞 (HUVEC) 进行了蛋白质和RNA测序分析.
操纵RCN1表达 (过度表达和沉默) 以研究其对ER压力标志物 (PERK,CHOP) 和内皮细胞功能的影响.
研究了TRIM11介导的全方位化对RCN1稳定性的作用.
对人类的DFU样本进行了RCN1水平和与疾病进展和治疗结果的相关性分析.

主要成果:

糖尿病小鼠的愈不良,血管生成减少,RCN1表达率降低.
糖脂毒性影响了HUVEC管体的形成,迁移和生存,与RCN1的下调有关.
过度表达RCN1减轻了由糖脂毒性或Thapsigargin (TG) 诱导的ER压力,而RCN1沉默则加剧了它.
通过TRIM11介导的全方位化影响了RCN1的稳定性和血管生成.
通过减少ER压力和增强血管生成,RCN1过度表达加速了小鼠的DFU愈合.
人体DFU样本中的低RCN1水平与破坏的ER蛋白和疾病严重程度相关.
在治疗后,RCN1水平在改善DFU愈合的患者中增加.

结论:

在糖尿病条件下,RCN1在维持内皮细胞功能和ER平衡方面发挥着至关重要的作用.
由RCN1抑制促成的糖脂毒性诱导的ER压力有助于内皮功能障碍和非愈合的DFU.
RCN1是促进糖尿病足愈合的有希望的治疗.

关键词:

细胞亡糖尿病足细胞内膜网应力内皮细胞内皮功能一个RCN

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