Plasma ACE2 activity is persistently elevated following SARS-CoV-2 infection: implications for COVID-19 pathogenesis and consequences
Sheila K. Patel, Jennifer A. Juno, Wen Shi Lee, Kathleen M. Wragg, P. Mark Hogarth, Stephen J. Kent, Louise M. Burrell
Source: Eur Respir J, 57 (5) 2003730; 10.1183/13993003.03730-2020
Abstract
Coronavirus disease 2019 (COVID-19) causes persistent endothelial inflammation, lung, cardiovascular, kidney and neurological complications, and thromboembolic phenomena of unclear pathogenesis [1]. Severe acute respiratory syndrome-coronavirus-2 (SARS-CoV-2) utilises the catalytic site of full-length membrane-bound angiotensin converting enzyme 2 (ACE2) for host cell entry [2], which is thought to downregulate membrane-bound ACE2, and thus contribute to ongoing inflammation due to loss of a degradative pathway for angiotensin II. In healthy individuals, ACE2 exists primarily in its membrane-bound form with very low levels of the catalytically active ectodomain of ACE2 present in the circulation [3]. However, in patients with cardiovascular disease, there is increased “shedding” of ACE2, and higher circulating levels are associated with downregulation of membrane-bound ACE2 [4].
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Sheila K. Patel, Jennifer A. Juno, Wen Shi Lee, Kathleen M. Wragg, P. Mark Hogarth, Stephen J. Kent, Louise M. Burrell. Plasma ACE2 activity is persistently elevated following SARS-CoV-2 infection: implications for COVID-19 pathogenesis and consequences. Eur Respir J, 57 (5) 2003730; 10.1183/13993003.03730-2020
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