코로나바이러스19 감염증과 안지오텐신전환효소2
Severe Acute Respiratory Syndrome-coronavirus 2 Inf
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A role of angiotensin-converting enzyme 2 (ACE2) in the coronavirus disease 2019 pandemic has been suggested, because it is the molecular receptor for severe acute respiratory syndrome-coronavirus 2 (SARS-CoV2). ACE2 is known to provide a protective effect for cardiac and vascular tissues, because it generally counteracts angiotensin II (Ang II) activity. ACE2 downregulation has been implicated in the pathogenesis of cardiovascular disease. ACE inhibitors and angiotensin receptor blockers may enhance ACE2 mRNA expression and enzyme activity. However, this has not been demonstrated in lung tissue. In the lungs, Ang II induces vasoconstriction to prevent ventilation perfusion mismatch, while also increasing vascular permeability (which can precipitate pulmonary edema). ACE2 is expressed in 0.67% of human lung cells, 80% of which are type 2 alveolar cells. Men (of all ethnicities) and Asian individuals have been shown to express higher levels of ACE2 than women and non-Asian individuals, respectively. However, there are no data from human studies indicating that high ACE2 expression increases the likelihood of SARS-CoV2 infection. In animal studies, an increase in Ang II caused by SARS-CoV2 or spike protein interactions, in turn due to ACE2 downregulation, has been identified as the key mechanism underlying lung injury. In human studies of SARS-CoV2 infection, ACE2 overexpression was shown to cause inflammatory apoptosis and a cytokine storm. The actions of ACE2 and Ang II in SARS-CoV2-infected vascular and lung tissues differ between animals and humans. ACE2 expression levels pre- and post-SARS-CoV2 infection should be differentiated.
Abstract
A role of angiotensin-converting enzyme 2 (ACE2) in the coronavirus disease 2019 pandemic has been suggested, because it is the molecular receptor for severe acute respiratory syndrome-coronavirus 2 (SARS-CoV2). ACE2 is known to provide a protective effect for cardiac and vascular tissues, because it generally counteracts angiotensin II (Ang II) activity. ACE2 downregulation has been implicated in the pathogenesis of cardiovascular disease. ACE inhibitors and angiotensin receptor blockers may enhance ACE2 mRNA expression and enzyme activity. However, this has not been demonstrated in lung tissue. In the lungs, Ang II induces vasoconstriction to prevent ventilation perfusion mismatch, while also increasing vascular permeability (which can precipitate pulmonary edema). ACE2 is expressed in 0.67% of human lung cells, 80% of which are type 2 alveolar cells. Men (of all ethnicities) and Asian individuals have been shown to express higher levels of ACE2 than women and non-Asian individuals, respectively. However, there are no data from human studies indicating that high ACE2 expression increases the likelihood of SARS-CoV2 infection. In animal studies, an increase in Ang II caused by SARS-CoV2 or spike protein interactions, in turn due to ACE2 downregulation, has been identified as the key mechanism underlying lung injury. In human studies of SARS-CoV2 infection, ACE2 overexpression was shown to cause inflammatory apoptosis and a cytokine storm. The actions of ACE2 and Ang II in SARS-CoV2-infected vascular and lung tissues differ between animals and humans. ACE2 expression levels pre- and post-SARS-CoV2 infection should be differentiated.
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