关键词: acute lung injury and acute respiratory distress syndrome renin angiotensin system viral infection

来  源:   DOI:10.2147/IDR.S265718   PDF(Sci-hub)   PDF(Pubmed)

Abstract:
The renin-angiotensin system (RAS) is the most important regulatory system of electrolyte homeostasis and blood pressure and acts through angiotensin-converting enzyme (ACE)/angiotensin II (Ang II)/Ang II type 1 (AT1) receptor axis and angiotensin-converting enzyme 2 (ACE2)/angiotensin (1-7)/MAS receptor axis. RAS dysfunction is related to the occurrence and development of acute lung injury (ALI) and acute respiratory distress syndrome (ARDS) and causes a serious prognosis and even death. ALI/ARDS can be induced by various ways, one of which is viral infections, such as SARS-CoV, SARS-CoV-2, H5N1, H7N9, and EV71. This article reviews the specific mechanism on how RAS dysfunction affects ALI/ARDs caused by viral infections. SARS-CoV and SARS-CoV-2 enter the host cells by binding with ACE2. H5N1 and H7N9 avian influenza viruses reduce the ACE2 level in the body, and EV71 increases Ang II concentration. Treatment with angiotensin-converting enzyme inhibitor and angiotensin AT1 receptor blocker can alleviate ALI/ARDS symptoms. This review provides suggestions for the treatment of lung injury caused by viral infections.
摘要:
肾素-血管紧张素系统(RAS)是电解质稳态和血压最重要的调节系统,并通过血管紧张素转换酶(ACE)/血管紧张素II(AngII)/AngII1型(AT1)受体轴和血管紧张素转换酶2(ACE2)/血管紧张素(1-7)/MAS受体轴发挥作用。RAS功能障碍与急性肺损伤(ALI)和急性呼吸窘迫综合征(ARDS)的发生、发展有关,导致严重的预后甚至死亡。ALI/ARDS可以通过各种方式诱发,其中之一是病毒感染,比如SARS-CoV,SARS-CoV-2、H5N1、H7N9和EV71。本文综述了RAS功能障碍如何影响病毒感染引起的ALI/ARDs的具体机制。SARS-CoV和SARS-CoV-2通过与ACE2结合进入宿主细胞。H5N1和H7N9禽流感病毒降低体内ACE2水平,EV71增加AngII浓度。血管紧张素转换酶抑制剂和血管紧张素AT1受体阻滞剂治疗可缓解ALI/ARDS症状。本综述为病毒感染引起的肺损伤的治疗提供建议。
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