血管紧张素Ⅱ引起的靶器官损伤与单核细胞趋化因子-1

Angiotensin Ⅱ-induced Target Organ Damage and Monocyte Chemoattractant Protein-1

肾素-血管紧张素系统(RAS)过度激活时,血管紧张素Ⅱ(AngⅡ)水平的升高在多种心血管疾病、肝脏、肾脏疾病的发病中具有重要的作用。研究表明,AngⅡ可以促进多种炎症因子的分泌,炎症因子参与了AngⅡ引起的靶器官损伤过程。其中单核细胞趋化因子-1(MCP-1)被认为是介导AngⅡ致靶器官损伤的一个关键因子,它与AngⅡ参与的多种疾病有关。AngⅡ通过激活核因子-kappa B(NF-κB)调控MCP-1的基因转录。除NF-κB之外,AngⅡ还可能通过多条信号途径调节MCP-1的表达。现对AngⅡ对MCP-1的调节,及MCP-1在介导AngⅡ的靶器官损伤中的作用等问题作一综述。

Increasing in angiotensin Ⅱ(AngⅡ) as renin-angiotensin system over activated plays a critical role in the pathogenesis of a wide spectrum of diseases,including cardiovascular diseases,liver and renal damages.Researches have suggested that the increased AngⅡ can promote productions of numerous inflammatory factors that mediated the target organ damage caused by AngⅡ.Among these factors,monocyte chemoattractant protein-1(MCP-1) is considered as the most important mediator of AngⅡ.It is associated with a number of diseases that AngⅡ is involved in.AngⅡ may modulate transcription of MCP-1 gene through activation of nuclear factor-kappa B(NF-κB).Additionally,some other signal pathways may participate in MCP-1 formation induced by AngⅡ.This paper briefly reviews the modulation of AngⅡ on MCP-1 and the action of MCP-1 in AngⅡ induced target organ damage.