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Editorial
. 2021 Apr;231(4):e13608.
doi: 10.1111/apha.13608. Epub 2021 Jan 7.

SARS-CoV-2 effects on the renin-angiotensin-aldosterone system, therapeutic implications

Qing Ye  1 , En Yin Lai  2   3 , Friedrich C Luft  4 , Pontus B Persson  3 , Jianhua Mao  1
Affiliations
Editorial

SARS-CoV-2 effects on the renin-angiotensin-aldosterone system, therapeutic implications

Qing Ye et al. Acta Physiol (Oxf). 2021 Apr.
No abstract available

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Conflict of interest statement

The authors declare no conflict of interest.

Figures

FIGURE 1
FIGURE 1
Possible effects of COVID‐19 on kidney RAS and its treatment. A, SARS‐CoV‐2 gains entry into the cell by binding to angiotensin‐converting enzyme 2 (ACE‐2) and weakens the activity of ACE‐2, then elevates angiotensin II (ANGII), which drives kidney injury by activating the angiotensin II type 1 receptor (AT1R), causing inflammation and fibrosis (left panel). The addition of angiotensin‐converting enzyme inhibitors (ACEIs) or angiotensin receptor blockers (ARBs) could increase ACE‐2 abundance and thus enhance viral entry, and diminish the production of ANGII. Enhanced angiotensin‐(1‐7) generation takes place by ACE‐2, which promotes the activation of Mas receptor (MasR), thus attenuating inflammation and fibrosis (right panel). B, SARS‐CoV‐2 gains entry into the cell by binding to angiotensin‐converting enzyme 2 (ACE‐2) (left panel). Human recombinant soluble ACE‐2 (hrsACE‐2) binds to Spike protein can reduce binding to ACE‐2 at the membrane, thus inhibiting SARS‐CoV‐2 internalization (right panel)
See this image and copyright information in PMC

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