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Comment
. 2020 Aug;15(5):885-887.
doi: 10.1007/s11739-020-02365-5. Epub 2020 May 18.

Antagonizing the renin-angiotensin-aldosterone system in the era of COVID-19

Riccardo Sarzani  1   2   3 , Federico Giulietti  4   5 , Chiara Di Pentima  4   5 , Andrea Filipponi  4   5 , Francesco Spannella  4   5
Affiliations
Comment

Antagonizing the renin-angiotensin-aldosterone system in the era of COVID-19

Riccardo Sarzani et al. Intern Emerg Med. 2020 Aug.
No abstract available

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Conflict of interest statement

The authors declare that they have no conflict of interest.

Figures

Fig. 1
Fig. 1
Schematic of the protective role of ACE2 and counter-regulatory renin–angiotensin–aldosterone system (RAAS) in lung injuries potentially leading to ARDS. ARB therapy, in animal models, counterbalances the down-regulation of ACE2, like the one caused by the SARS-CoV-2 infection in lung. ARB could lead to an increase in the protective components of the RAAS (by reduction of Ang II/AT1R stimulation, increase in Ang II substrate, increase in Ang II and Ang A conversion in Ang 1–7 and Alamandine, respectively) with potential prevention and/or attenuation of ARDS. ACE2: angiotensin-converting-enzyme 2; Ang: angiotensin; ARB: angiotensin II type 1 receptor blockers; AT1R: angiotensin II type 1 receptor; AT2R: angiotensin II type 2 receptor; SARS-CoV-2: severe acute respiratory syndrome coronavirus-2; MasR: Mas receptor; MrgD: Mas-related G protein-coupled receptor D; AD: aspartate decarboxylase; ARDS: acute respiratory distress syndrome
See this image and copyright information in PMC

Comment on

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