PMC:7252096 / 66545-68122 JSONTXT

{"target":"http://pubannotation.org/docs/sourcedb/PMC/sourceid/7252096","sourcedb":"PMC","sourceid":"7252096","source_url":"https://www.ncbi.nlm.nih.gov/pmc/7252096","text":"ACE2 is a central component of the renin-angiotensin system, which has emerged as a key regulator of sterile- or microbially induced lung pathology (Imai et al., 2005). In brief, ACE cleaves angiotensin I to generate angiotensin II (Skeggs et al., 1980). Angiotensin II then acts to drive acute lung injury through various mechanisms, including increased vascular permeability (Imai et al., 2005). Amounts of angiotensin II in humans and mice are elevated during influenza infection, and ACE2 exerts tissue-protective functions by reducing amounts of angiotensin II (Zou et al., 2014). Binding of SARS-CoV-S to mouse ACE2 in vivo reduced ACE2 expression leading to acute acid-aspiration-induced lung failure (Kuba et al., 2005). Depending on the questions asked in future work, there are mouse models available on the basis of transgenic expression of human ACE2 (required for overt infectious pathology of SARS-CoV in mice), there are established NHP models available of SARS-CoV infection in M. fascicularis and C. aethiops, and early reports suggest symptomatic infection in M. mulatta and M. fascicularis models for SARS-CoV-2 (Bao et al., 2020, McCray et al., 2007, Munster et al., 2020, Rockx et al., 2020, Smits et al., 2011). For example, examining the efficacy of recombinant human ACE2 to act as a decoy receptor or the effect of “ACE inhibitors” in patients with, or at risk for, COVID-19 will require careful experimentation in appropriate models together with well-controlled clinical trials (Hofmann et al., 2004, Monteil et al., 2020, Vaduganathan et al., 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