SUMMARY Using serial analysis of myocardial gene expression employing endomyocardial biopsy starting material in a dilated cardiomyopathy cohort, we show that the SARS-CoV-2 cardiac myocyte receptor ACE2 is upregulated with… Click to show full abstract
SUMMARY Using serial analysis of myocardial gene expression employing endomyocardial biopsy starting material in a dilated cardiomyopathy cohort, we show that the SARS-CoV-2 cardiac myocyte receptor ACE2 is upregulated with remodeling and with reverse remodeling down-regulates into the normal range. The proteases responsible for virus-cell membrane fusion were expressed but not regulated with remodeling. In addition, a new candidate for CoV-2 cell binding and entry was identified, the integrin ITGA5. The upregulation in ACE2 in remodeled LVs may explain worse outcomes in COVID-19 patients with underlying myocardial disorders, and counteracting ACE2 upregulation is a possible therapeutic approach to minimizing cardiac damage.
               
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