败血症
髓样
肾素-血管紧张素系统
血管紧张素转化酶2
医学
血管紧张素II
髓系细胞
氧化应激
巨噬细胞极化
炎症
药理学
下调和上调
内分泌学
内科学
血压
巨噬细胞
化学
体外
生物化学
疾病
2019年冠状病毒病(COVID-19)
传染病(医学专业)
基因
作者
Jiaxin Li,Xue Xiao,Fei Teng,Huihua Li
出处
期刊:Redox biology
[Elsevier]
日期:2024-02-01
卷期号:69: 103004-103004
被引量:2
标识
DOI:10.1016/j.redox.2023.103004
摘要
Angiotensin converting enzyme 2 (ACE2) is a new identified member of the renin-angiotensin-aldosterone system (RAAS) that cleaves angiotensin II (Ang II) to Ang (1-7), which exerts anti-inflammatory and antioxidative activities via binding with Mas receptor (MasR). However, the functional role of ACE2 in sepsis-related hypotension remains unknown. Our results indicated that sepsis significantly reduced blood pressure and led to disruption between ACE-Ang II and ACE2-Ang (1-7) balance. ACE2 knock-in mice exhibited improved sepsis-induced mortality, hypotension and vascular dysfunction, while ACE2 knockout mice exhibited the opposite effects. Bone marrow transplantation and in vitro experiments confirmed that myeloid ACE2 exerted a protective role by suppressing oxidative stress, NO production and macrophage polarization via the Ang (1-7)-MasR-NF-κB and STAT1 pathways. Thus, ACE2 on myeloid cells could protect against sepsis-mediated hypotension and vascular dysfunction, and upregulating ACE2 may represent a promising therapeutic option for septic patients with hypotension.
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