Impact of renin–angiotensin–aldosterone system inhibitors on COVID-19

被引:0
作者
Yasushi Matsuzawa
Kazuo Kimura
Hisao Ogawa
Kouichi Tamura
机构
[1] Yokohama City University Medical Center,Division of Cardiology
[2] Yokosuka City Hospital,Department of Medical Science and Cardiorenal Medicine
[3] Kumamoto University,undefined
[4] Yokohama City University Graduate School of Medicine,undefined
来源
Hypertension Research | 2022年 / 45卷
关键词
Coronavirus disease 2019; Renin–angiotensin system; Angiotensin-converting enzyme 2; Angiotensin-converting enzyme inhibitor; Angiotensin II type-1 receptor blocker;
D O I
暂无
中图分类号
学科分类号
摘要
Since the onset of the coronavirus disease 2019 (COVID-19) pandemic, the possible roles of renin–angiotensin system (RAS) inhibitors in COVID-19 have been debated as favorable, harmful, or neutral. Angiotensin-converting enzyme 2 (ACE2) not only is the entry route of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection but also triggers a major mechanism of COVID-19 aggravation by promoting tissue RAS dysregulation, which induces a hyperinflammatory state in several organs, leading to lung injury, hematological alterations, and immunological dysregulation. ACE inhibitors and angiotensin II type-1 receptor blockers (ARBs) inhibit the detrimental hyperactivation of the RAS by SARS-CoV-2 and increase the expression of ACE2, which is a counter-regulator of the RAS. Several studies have investigated the beneficial profile of RAS inhibitors in COVID-19; however, this finding remains unclear. Further prospective studies are warranted to confirm the role of RAS inhibitors in COVID-19. In this review, we summarize the potential effects of RAS inhibitors that have come to light thus far and review the impact of RAS inhibitors on COVID-19.
引用
收藏
页码:1147 / 1153
页数:6
相关论文
共 147 条
  • [1] Hoffmann M(2020)SARS-CoV-2 cell entry depends on ACE2 and TMPRSS2 and is blocked by a clinically proven protease inhibitor Cell 181 271-80 e8
  • [2] Kleine-Weber H(2004)The nucleocapsid protein of the SARS coronavirus is capable of self-association through a C-terminal 209 amino acid interaction domain Biochem Biophys Res Commun 317 1030-6
  • [3] Schroeder S(2020)ACE2 the Janus-faced protein - from cardiovascular protection to severe acute respiratory syndrome-coronavirus and COVID-19 Clin Sci 134 747-50
  • [4] Krüger N(2021)Downregulation of ACE2 expression by SARS-CoV-2 worsens the prognosis of KIRC and KIRP patients via metabolism and immunoregulation Int J Biol Sci 17 1925-39
  • [5] Herrler T(2003)The role of ACE2 in cardiovascular physiology Trends Cardiovasc Med 13 93-101
  • [6] Erichsen S(2010)Trilogy of ACE2: a peptidase in the renin-angiotensin system, a SARS receptor, and a partner for amino acid transporters Pharmacol Ther 128 119-28
  • [7] Surjit M(2013)Multiple functions of angiotensin-converting enzyme 2 and its relevance in cardiovascular diseases Circ J 77 301-8
  • [8] Liu B(2005)Effect of angiotensin-converting enzyme inhibition and angiotensin II receptor blockers on cardiac angiotensin-converting enzyme 2 Circulation 111 2605-10
  • [9] Kumar P(2015)Urinary angiotensin-converting enzyme 2 in hypertensive patients may be increased by olmesartan, an angiotensin II receptor blocker Am J Hypertens 28 15-21
  • [10] Chow VT(2020)Association of use of angiotensin-converting enzyme inhibitors and angiotensin II receptor blockers with testing positive for coronavirus disease 2019 (COVID-19) JAMA Cardiol. 5 1020-6