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Editorial
. 2020 Jun 8;2(1):E3-E6.
doi: 10.1530/VB-20-0008. eCollection 2020.

Cardiovascular complications of COVID-19: evidence, misconceptions, and new opportunities

Paolo Madeddu  1
Affiliations
Editorial

Cardiovascular complications of COVID-19: evidence, misconceptions, and new opportunities

Paolo Madeddu. Vasc Biol. .
No abstract available

PubMed Disclaimer

Conflict of interest statement

The author declares that there is no conflict of interest that could be perceived as prejudicing the impartiality of this editorial.

Figures

Figure 1
Figure 1
ACE2 downregulation by SARS-CoV-2 induces pericyte damage and microvascular dysfunction. (A) SARS-CoV-2 uses the ACE2 receptor for entry and the serine protease TMPRSS2 for S protein priming. (B) ACE2-mediated cardiovascular protection is lost following endocytosis of the receptor along with SARS-CoV-2 viral particles. (C) Unopposed ACE activity leads to Ang II generation with increased activity of angiotensin 1 receptors (AT1R) at the cost of ACE2/Ang 1–7 driven pathways. (D) This leads to increased reactive oxygen species (ROS), vasoconstriction, vascular permeability, oxidative stress, and inflammation. Moreover, ACE2 downregulation results in increased level of Des-Arg9-bradykinin (normally degraded by ACE2) which through the kinin receptor B1 (B1R) causes vascular leakage and inflammation. (E) ADAM17 mediated proteolytic cleavage of ACE2 is upregulated by endocytosed SARS-CoV-2 spike proteins. Activation of the AT1R by elevated Ang II levels also further increases ADAM17 activity. Soluble ACE2 can act as a blocking receptor for SARS-CoV-2. (F) After replication and cellular damage, the virus spreads to other cells causing incremental injury and vascular dysfunction. Alternatively, if the virus does not reach the heart, viral particles and proteins could do so, activating the described signalling pathway.
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