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

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

| PRJNA986061 | ENA

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

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

| PRJNA986067 | ENA

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

Project description:SARS-CoV-2 infection triggers pro-atherogenic inflammatory responses in human coronary [MAC_FOAM-RNAseq]

| PRJNA986066 | ENA

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.

2023-08-18 | GSE235435 | GEO

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

2023-08-18 | GSE235436 | GEO

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

2023-08-18 | GSE235433 | GEO

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.

| S-EPMC10702930 | biostudies-literature

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

Project description:Regulation of coding and non-coding genes is studied from primary human aortic endothelial cells (HAECs), venous endothelial cells (HUVECs), aortic smooth muscle cells (HASMCs) and macrophages (CD14+) under pro-atherogenic stimuli (hypoxia, oxPAPC and hypoxia+oxPAPC) by integrating three different sequencing techinques: GRO-seq, miRNA-seq and RNA-seq

2020-06-17 | GSE136813 | GEO

Mitochondrial 3243A > G mutation confers pro-atherogenic and pro-inflammatory properties in MELAS iPS derived endothelial cells

Project description:Mitochondrial 3243A > G mutation confers pro-atherogenic and pro-inflammatory properties in MELAS iPS derived endothelial cells

| PRJNA524862 | ENA

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