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Linking ACE2 and angiotensin II to pulmonary immunovascular dysregulation in SARS-CoV-2 infection.
Seltzer, S.
  • Seltzer S; School of Medicine, University College Cork, Cork, Ireland. Electronic address: 116100016@umail.ucc.ie.
Int J Infect Dis ; 101: 42-45, 2020 Dec.
Article in English | MEDLINE | ID: covidwho-779011
ABSTRACT
Angiotensin-converting enzyme 2 (ACE2) is the receptor of the novel coronavirus, severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), the causative agent of the coronavirus disease 2019 (COVID-19) pandemic. ACE2 has been shown to be down-regulated during coronaviral infection, with implications for circulatory homeostasis. In COVID-19, pulmonary vascular dysregulation has been observed resulting in ventilation perfusion mismatches in lung tissue, causing profound hypoxemia. Despite the loss of ACE2 and raised circulating vasoconstrictor angiotensin II (AngII), COVID-19 patients experience a vasodilative vasculopathy. This article discusses the interplay between the immune system and pulmonary vasculature and how SARS-CoV-2-mediated ACE2 disruption and AngII may contribute to the novel vascular pathophysiology of COVID-19.
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Full text: Available Collection: International databases Database: MEDLINE Main subject: Vascular Diseases / Angiotensin II / Angiotensin-Converting Enzyme 2 / SARS-CoV-2 / COVID-19 / Lung Topics: Long Covid Limits: Humans Language: English Journal: Int J Infect Dis Journal subject: Communicable Diseases Year: 2020 Document Type: Article

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Full text: Available Collection: International databases Database: MEDLINE Main subject: Vascular Diseases / Angiotensin II / Angiotensin-Converting Enzyme 2 / SARS-CoV-2 / COVID-19 / Lung Topics: Long Covid Limits: Humans Language: English Journal: Int J Infect Dis Journal subject: Communicable Diseases Year: 2020 Document Type: Article