id	author	title	date	pages	extension	mime	words	sentences	flesch	summary	cache	txt
cord-324919-ciamusjs	Scialo, Filippo	ACE2: The Major Cell Entry Receptor for SARS-CoV-2	2020-11-10		.txt	text/plain	5356	257	42	Since the beginning of the COVID-19 pandemic, hypertension and diabetes have been correlated with higher risk of mortality, and initial reports speculated that angiotensin converting enzyme inhibitors (ACEi) and angiotensin receptor blockers (ARBs), which are commonly used therapeutic agents for these conditions, would up-regulate ACE2 expression, thus increasing the risk of severe illness [37] . Binding of S1 subunit of the Spike protein of SARS-CoV-2 to the ACE2 receptor triggers the cleavage of ACE2 by ADAM17/tumor necrosis factorconverting enzyme (TACE) at the ectodomain sites [41] and a soluble form that retains its catalytic activity (sACE2) is produced [42] . ACE2 shedding can be stimulated by proinflammatory cytokines such as IL-1β and tumor necrosis factor (TNF)-α, and endotoxin [47] that could result in a positive effect reducing SARS-CoV-2 entry, but at the same time, may cause an increase in AngII and further activation of the AngII/AT1R axis worsening inflammation (discussed below) (Fig. 1) . Tumor necrosis factor-alpha convertase (ADAM17) mediates regulated ectodomain shedding of the severe-acute respiratory syndrome-coronavirus (SARS-CoV) receptor, angiotensin-converting enzyme-2 (ACE2)	./cache/cord-324919-ciamusjs.txt	./txt/cord-324919-ciamusjs.txt