Human cardiosphere-derived stromal cells exposed to SARS-CoV-2 evolve into hyper-inflammatory/pro-fibrotic phenotype and produce infective viral particles depending on the levels of ACE2 receptor expression.
Alessandra AmendolaGloria GaroffoloPaola SongiaRoberta NardacciSilvia FerrariGiacomo BernavaPaola CanzanoVeronika MyasoedovaFrancesca ColavitaConcetta CastillettiGiuseppe SbernaMaria Rosaria CapobianchiMauro PiacentiniMarco AgrifoglioGualtiero Ivanoe ColomboPoggio PaoloMaurizio PescePublished in: Cardiovascular research (2021)
Our findings indicate that cardiac stromal cells are susceptible to SARS-CoV-2 infection and produce variable viral yields depending on the extent of cellular ACE2 receptor expression. Interestingly, these cells also evolved towards hyper-inflammatory/pro-fibrotic phenotypes independently of ACE2 levels. Thus, SARS-CoV-2 infection of myocardial stromal cells could be involved in cardiac injury and explain the high number of complications observed in severe cases of COVID-19.
Keyphrases
- sars cov
- respiratory syndrome coronavirus
- angiotensin converting enzyme
- left ventricular
- angiotensin ii
- induced apoptosis
- oxidative stress
- endothelial cells
- systemic sclerosis
- idiopathic pulmonary fibrosis
- anti inflammatory
- coronavirus disease
- cell cycle arrest
- risk factors
- heart failure
- endoplasmic reticulum stress