慢性病将静脉转化为一个专门的免疫内分泌器官,增加了MYCN-AP1信号传输
Fatma Saaoud1, Laisel Martinez2, Yifan Lu1
1Center for Cardiovascular Research, Department of Cardiovascular Sciences, Lewis Katz School of Medicine at Temple University, Philadelphia, PA 19140, USA.
慢性病 (CKD) 将静脉转化为免疫器官,改变基因表达,并通过促进炎症和纤维化来为动脉静脉 (AVF) 失败做准备.
科学领域:
- 血管生物学 血管生物学
- 腎臟病學 (nephrology) 是一種醫學專業.
- 免疫学 免疫学 免疫学
背景情况:
- 患有末期病 (ESRD) 的患者通常需要血液透析,利用上肢静脉产生动脉静脉 (AVF).
- 慢性病 (CKD) 对静脉转录组的影响及其对AVF衰竭的倾向仍然在很大程度上未被探索.
研究的目的:
- 研究CKD如何改变静脉的基因表达特征.
- 为了确定在CKD中静脉重编程背后的分子机制,这可能导致AVF失败.
主要方法:
- 使用大量RNA测序进行转录组分析.
- 在48名CKD患者和20名非CKD对照者之间对静脉基因表达的比较.
主要成果:
- 慢性瘤可以调节免疫和分泌基因,将静脉转化为免疫内分泌器官.
- 在CKD静脉中,先天性免疫反应,细胞间通信 (例如CX3CR1信号传递) 和免疫代谢重编程都得到了增强.
- 纤维化过程,细胞死亡/生存途径以及与胚胎发育有关的转录因子被重新编程,使静脉易于发生AVF失败.
结论:
- 慢性瘤显著重编程静脉转录组,促进免疫激活和纤维化.
- 这些转录组变化为CKD患者的静脉功能障碍和AVF衰竭提供了洞察力.
- 慢性瘤患者的静脉表现出免疫内分泌器官的特征,影响血管细胞的分化和功能.
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