March 6, 2024Physiological ResearchOpen Access

Angiotensin I and II Stimulate Cell Invasion of SARS-CoV-2: Potential Mechanism via Inhibition of ACE2 Arm of RAS

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Angiotensin I and II stimulate SARS-CoV-2 spike pseudovirus entry into host cells by binding to the catalytic pocket of ACE2 without requiring angiotensin type I receptors.
Infectivity increased by 129.74% at 100 µM of Ang II, demonstrating tenfold higher efficiency than Ang I in promoting SARS-CoV-2 spike pseudovirus cellular invasion.
Co-incubation assays in HEK-ACE2 and Vero E6 cells show altered enzyme metabolism, highlighting invasion risks in patients with an overactivated renin-angiotensin system.

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Implication

In vitro study reveals that angiotensin peptides stimulate SARS-CoV-2 entry in HEK-ACE2 and Vero E6 cells, highlighting invasion risks in patients with an overactivated renin-angiotensin system.

Cite This Study

Zórad et al. (2024) studied this question.

synapsesocial.com/papers/68e758b6b6db6435876d00c1 https://doi.org/10.33549/physiolres.935198

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Implication

In vitro study reveals that angiotensin peptides stimulate SARS-CoV-2 entry in HEK-ACE2 and Vero E6 cells, highlighting invasion risks in patients with an overactivated renin-angiotensin system.

Angiotensin I and II Stimulate Cell Invasion of SARS-CoV-2: Potential Mechanism via Inhibition of ACE2 Arm of RAS

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Discussion

Implication

Cite This Study

Angiotensin I and II Stimulate Cell Invasion of SARS-CoV-2: Potential Mechanism via Inhibition of ACE2 Arm of RAS

Key Points

Discussion

Implication

Cite This Study

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