Plasma ACE2 activity is persistently elevated following SARS-CoV-2 infection: implications for COVID-19 pathogenesis and consequences

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].
Source: European Respiratory Journal - Category: Respiratory Medicine Authors: Tags: Original Articles: Research letters Source Type: research