Angiotensin-converting enzyme 2 (ACE2) has been identified as the host entry receptor for the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) responsible for the COVID-19 pandemic. ACE2 is a regulatory enzyme of the renin-angiotensin system and has protective functions in many cardiovascular, pulmonary and metabolic diseases. This review summarizes available murine models with systemic or organ-specific deletion of ACE2, or with overexpression of murine or human ACE2. The purpose of this review is to provide researchers with the genetic tools available for further understanding of ACE2 biology and for the investigation of ACE2 in the pathogenesis and treatment of COVID-19. Angiotensin-converting enzyme 2 (ACE2) is a cell surface enzyme previously shown to mediate SARS-CoV, and now SARS-CoV-2, entry into host cells. Here the authors review existing mouse ACE2 models expressing humanized, transgenic, knockout, knockin, conditional and reporter alleles to provide a toolbox for COVID-19 research.
【저자키워드】 viral infection, Infection, Experimental models of disease, genetic engineering, 【초록키워드】 COVID-19, Treatment, SARS-CoV-2, ACE2, coronavirus, Pathogenesis, SARS-CoV, COVID-19 pandemic, Genetic, renin-angiotensin system, human ACE2, Regulatory, murine model, reporter, function, Protective, Metabolic diseases, host cells, acute respiratory syndrome, enzyme, entry receptor, allele, overexpression, COVID-19 research, researcher, murine, Host, transgenic, humanized, Cell, shown, responsible, expressing, organ-specific, 【제목키워드】 ACE2, Research,