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SARS-CoV-2 infection triggers pro-atherogenic inflammatory responses in human coronary [scRNA-seq]

ABSTRACT: SARS-CoV-2 infection triggers pro-atherogenic inflammatory responses in human coronary [scRNA-seq]

PROVIDER: PRJNA986069 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR24981503.fastq.gz	Fastqsanger.gz
	SRR24981504.fastq.gz	Fastqsanger.gz
	SRR24981505.fastq.gz	Fastqsanger.gz
	SRR24981506.fastq.gz	Fastqsanger.gz
	SRR24981507.fastq.gz	Fastqsanger.gz

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SARS-CoV-2 infection triggers pro-atherogenic inflammatory responses in human coronary

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SARS-CoV-2 infection triggers pro-atherogenic inflammatory responses in human coronary [plaque]

Project description:COVID-19 patients present higher risk for myocardial infarction (MI), acute coronary syndrome, and stroke for up to 1 year after SARS-CoV-2 infection. While the systemic inflammatory response to SARS-CoV-2 infection likely contributes to this increased cardiovascular risk, whether SARS35 CoV-2 directly infects the coronary vasculature and attendant atherosclerotic plaques to locally promote inflammation remains unknown. Here, we report that SARS-CoV-2 viral RNA (vRNA) is detectable and the virus replicates in coronary atherosclerotic lesions taken at autopsy from patients with severe COVID-19.

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SARS-CoV-2 infection triggers pro-atherogenic inflammatory responses in human coronary [scRNA-seq]

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SARS-CoV-2 infection triggers pro-atherogenic inflammatory responses in human coronary

Project description:This SuperSeries is composed of the SubSeries listed below.

2023-08-18 | GSE235437 | GEO

SARS-CoV-2 infection triggers pro-atherogenic inflammatory responses in human coronary vessels.

Project description:Patients with coronavirus disease 2019 (COVID-19) present increased risk for ischemic cardiovascular complications up to 1 year after infection. Although the systemic inflammatory response to severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection likely contributes to this increased cardiovascular risk, whether SARS-CoV-2 directly infects the coronary vasculature and attendant atherosclerotic plaques remains unknown. Here we report that SARS-CoV-2 viral RNA is detectable and replicates in coronary lesions taken at autopsy from severe COVID-19 cases. SARS-CoV-2 targeted plaque macrophages and exhibited a stronger tropism for arterial lesions than adjacent perivascular fat, correlating with macrophage infiltration levels. SARS-CoV-2 entry was increased in cholesterol-loaded primary macrophages and dependent, in part, on neuropilin-1. SARS-CoV-2 induced a robust inflammatory response in cultured macrophages and human atherosclerotic vascular explants with secretion of cytokines known to trigger cardiovascular events. Our data establish that SARS-CoV-2 infects coronary vessels, inducing plaque inflammation that could trigger acute cardiovascular complications and increase the long-term cardiovascular risk.

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NRF2 is a key regulator of endothelial miRNA expression under pro-atherogenic stimuli

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