Plasma ACE2 activity is persistently elevated following SARS-CoV-2 infection: implications for COVID-19 pathogenesis and consequences
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Open Access
- 21 January 2021
- journal article
- letter
- Published by European Respiratory Society (ERS) in European Respiratory Journal
- Vol. 57 (5), 2003730
- https://doi.org/10.1183/13993003.03730-2020
Abstract
COVID-19 causes persistent endothelial inflammation, lung, cardiovascular, kidney and neurological complications as well as thromboembolic phenomena of unclear pathogenesis [1]. 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].Funding Information
- State Government of Victoria
- Medical Research Future Fund (1175865 and 2002073)
- National Health and Medical Research Council (1149990, 1055214, 145303)
- ARC Centre of Excellence in Convergent Bio-Nano Science and Technology (140100036)
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