Key result
In rats with heart failure, ACE2 and furin were overexpressed in pulmonary, cardiac, and renal tissues, while TMPRSS2 and ADAM17 were downregulated compared to sham controls.
Why the study?
Expression of ACE2 in pulmonary, cardiac, and renal systems in CHF has not been thoroughly studied, despite CHF predisposing to COVID-19 severity and ACE2 acting alongside furin, TMPRSS2, and ADAM17 in SARS-CoV-2 infection.
Does heart failure alter the expression of SARS-CoV-2 entry-related proteins (ACE2, furin, TMPRSS2, ADAM17) in pulmonary, cardiac, and renal tissues in a rat model?
Population
Male Sprague Dawley rats with surgical aorto-caval fistula-induced CHF and sham controls
Comparison
Compensated CHF vs decompensated CHF vs sham-operated controls
Design
Animal experimental study
Follow-up
One week after surgery
Authors
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Experimental HF alters ACE2-related enzymes; hypothesis-generating for COVID-19 links and requires human confirmation.
Does heart failure alter the expression of SARS-CoV-2 entry-related proteins (ACE2, furin, TMPRSS2, ADAM17) in pulmonary, cardiac, and renal tissues in a rat model?
In a rat model of heart failure, ACE2 and furin are overexpressed while TMPRSS2 and ADAM17 are downregulated, suggesting complex alterations in SARS-CoV-2 entry proteins that may influence COVID-19 susceptibility.
Khoury et al. (2021) studied Congestive heart failure (CHF). Heart failure (surgical aorto-caval fistula) vs. Sham-operated rats was evaluated on Expression of ACE2, furin, TMPRSS2 and ADAM17 in the lung, heart and kidneys. In rats with heart failure, ACE2 and furin were overexpressed in pulmonary, cardiac, and renal tissues, while TMPRSS2 and ADAM17 were downregulated compared to sham controls.
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