ACE2 Target Analysis Report Summary
About the Target
Based on the provided context information, here are some key viewpoints related to ACE2:
Endothelial Dysfunction: ACE2 depletion caused by the binding of SARS-CoV-2 to ACE2 receptors on endothelial cells leads to endothelial dysfunction, including vasoconstriction, oxidative stress, and inflammation [1].
Cerebrovascular Complications: The binding of SARS-CoV-2 to ACE2 receptors on the endothelial cells of large arteries and subsequent endocytosis into the brain can contribute to cerebrovascular complications [1].
Proinflammatory and Prothrombotic Effects: Dysfunctional ACE2 due to SARS-CoV-2 binding can lead to the accumulation of Angiotensin II, causing proinflammatory, prothrombotic, fibrotic, and vasoconstrictive effects [3].
Role of Heparin: Heparin, used as an anticoagulant, not only inhibits coagulation but also reduces virus binding to cell surfaces by decreasing the accessibility of heparan sulfate proteoglycan, potentially affecting infectivity [4].
Mechanisms of SARS-CoV-2 Transmission: SARS-CoV-2 gains entry to host cells by binding to ACE2 receptors on lung epithelial cells and directly invading endothelial expressed ACE-2. This can lead to thrombosis, activation of inflammatory responses, and recruitment of platelets and leukocytes [5].
Please note that the viewpoints have been derived directly from the provided context information and are not influenced by prior knowledge.
Based on the provided context information, several key viewpoints can be extracted regarding ACE2:
ACE2 is a key effector in the regulatory renin-angiotensin system (RAS) that counteracts the actions of the classical RAS and reduces the risk of cardiovascular diseases. It has been found to play a protective role by converting Angiotensin II (Ang II) to Ang (1-7), which has vasodilatory effects and contributes to maintaining vascular tone [7].
However, in the presence of SARS-CoV-2 infection, the virus attaches to ACE2 receptors, leading to internalization or cleavage of ACE2. This results in downregulation of the regulatory RAS and overactivation of the classical RAS, driving vascular dysfunction, inflammation, oxidative stress, and CNS injury in COVID-19 [7].
Imbalance between ACE and ACE2 activities occurs in comorbid patients with conditions such as hypertension, hyperglycemia, and chronic kidney disease. ACE activity is higher, leading to the accumulation of Ang II, while ACE2 activity is impaired [10]. This imbalance can contribute to endothelial dysfunction, oxidative stress, hypertension, and various organ disorders [10].
ACE2 expression is regulated by androgen signaling, and androgen suppression through androgen receptor (AR) signaling can decrease ACE2 expression. The binding of SARS-CoV-2 to ACE2 may be affected by androgen regulation, potentially influencing the severity of infection [9].
Targeting the RAS-axes, such as using angiotensin receptor blockers (ARBs), may be a potential strategy for improving the clinical outcomes of COVID-19 patients [10].
In summary, ACE2 plays a crucial role in the regulatory RAS and is involved in maintaining vascular tone and protecting against cardiovascular diseases. However, in the context of SARS-CoV-2 infection, ACE2 downregulation and imbalance in ACE and ACE2 activities can lead to vascular dysfunction, inflammation, and organ damage. Understanding the role of ACE2 and its regulation may provide insights into potential therapeutic strategies for COVID-19.
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Note: If you are interested in the full version of this target analysis report, or if you'd like to learn how our AI-powered BDE-Chem can design therapeutic molecules to interact with the ACE2 target at a cost 90% lower than traditional approaches, please feel free to contact us at BD@silexon.ai.
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