In:
PeerJ, PeerJ, Vol. 9 ( 2021-10-08), p. e12262-
Abstract:
Coronavirus disease 2019 (COVID-19) is caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), which can infect several organs, especially impacting respiratory capacity. Among the extrapulmonary manifestations of COVID-19 is myocardial injury, which is associated with a high risk of mortality. Myocardial injury, caused directly or indirectly by SARS-CoV-2 infection, can be triggered by inflammatory processes that lead to damage to the heart tissue. Since one of the hallmarks of severe COVID-19 is the “cytokine storm”, strategies to control inflammation caused by SARS-CoV-2 infection have been considered. Cannabinoids are known to have anti-inflammatory properties by negatively modulating the release of pro-inflammatory cytokines. Herein, we investigated the effects of the cannabinoid agonist WIN 55,212-2 (WIN) in human iPSC-derived cardiomyocytes (hiPSC-CMs) infected with SARS-CoV-2. WIN did not modify angiotensin-converting enzyme II protein levels, nor reduced viral infection and replication in hiPSC-CMs. On the other hand, WIN reduced the levels of interleukins six, eight, 18 and tumor necrosis factor-alpha (TNF-α) released by infected cells, and attenuated cytotoxic damage measured by the release of lactate dehydrogenase (LDH). Our findings suggest that cannabinoids should be further explored as a complementary therapeutic tool for reducing inflammation in COVID-19 patients.
Type of Medium:
Online Resource
ISSN:
2167-8359
DOI:
10.7717/peerj.12262/fig-1
DOI:
10.7717/peerj.12262/fig-2
DOI:
10.7717/peerj.12262/fig-3
DOI:
10.7717/peerj.12262/supp-1
DOI:
10.7717/peerj.12262/supp-2
DOI:
10.7717/peerj.12262/supp-3
DOI:
10.7717/peerj.12262/supp-4
DOI:
10.7717/peerj.12262/supp-5
Language:
English
Publisher:
PeerJ
Publication Date:
2021
detail.hit.zdb_id:
2703241-3
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