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ACE2 is an important enzymatic component of the renin-angiotensin system (RAS) expressed in the lung and other organs. The peptidase regulates the levels of the peptide hormones Ang II and Ang-(1\u20137), which have distinct and opposing actions to one another, as well as other cardiovascular peptides. A potential consequence of severe acute respiratory syndrome-related coronavirus-2 infection is reduced ACE2 activity by internalization of the viral-ACE2 complex and subsequent activation of the RAS (higher ratio of Ang II:Ang-[1\u20137]) that may exacerbate the acute inflammatory events in COVID-19 patients and possibly contribute to the effects of long COVID-19. Moreover, COVID-19 patients present with an array of autoantibodies to various components of the RAS including the peptide Ang II, the enzyme ACE2, and the AT\n                    <jats:sub>1<\/jats:sub>\n                    AT\n                    <jats:sub>2<\/jats:sub>\n                    and Mas receptors. Greater disease severity is also evident in male COVID-19 patients, which may reflect underlying sex differences in the regulation of the 2 distinct functional arms of the RAS. The current review provides a critical evaluation of the evidence for an activated RAS in COVID-19 subjects and whether this system contributes to the greater severity of severe acute respiratory syndrome-related coronavirus-2 infection in males as compared with females.\n                  <\/jats:p>","DOI":"10.1161\/circresaha.123.321883","type":"journal-article","created":{"date-parts":[[2023,5,11]],"date-time":"2023-05-11T14:00:17Z","timestamp":1683813617000},"page":"1320-1337","update-policy":"https:\/\/doi.org\/10.1161\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":32,"title":["Renin-Angiotensin System and Sex Differences in COVID-19: A Critical Assessment"],"prefix":"10.1161","volume":"132","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-5869-6037","authenticated-orcid":true,"given":"Mark C.","family":"Chappell","sequence":"first","affiliation":[{"name":"Hypertension and Vascular Research Center, Wake Forest University School of Medicine, Winston-Salem, 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