PMC:7121452 / 10653-12137 JSONTXT

{"target":"https://pubannotation.org/docs/sourcedb/PMC/sourceid/7121452","sourcedb":"PMC","sourceid":"7121452","source_url":"https://www.ncbi.nlm.nih.gov/pmc/7121452","text":"Dysregulated ACE2 may theoretically also attenuate cardioprotection in the context of myocardial involvement and abnormal pulmonary hemodynamics52,53 in Covid-19. Markers of myocardial injury have been shown to be elevated during the disease course of Covid-1954 and to increase rapidly with clinical deterioration and preceding death.14 Many viruses are cardiotropic, and subclinical viral myocarditis is commonly seen in viremia associated with a wide range of infectious agents. ACE2 has a well-recognized role in myocardial recovery and injury response; in one study, ACE2 knockout in animal models contributed to adverse left ventricular remodeling in response to acute injury driven by angiotensin II.55 In autopsies of patients who died from SARS, 35% of heart samples showed the presence of viral RNA, which in turn was associated with reduced ACE2 protein expression.56 Administration of recombinant ACE2 normalizes angiotensin II levels in human explanted hearts with dilated cardiomyopathy.57 These hypotheses have prompted trials to test whether the provision of recombinant ACE2 protein may be beneficial in restoring balance to the RAAS network and potentially preventing organ injury (ClinicalTrials.gov number, NCT04287686). In addition, paired trials of losartan as a treatment for Covid-19 are being conducted among patients who have not previously received treatment with a RAAS inhibitor and are either hospitalized (NCT04312009) or not hospitalized 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