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Human cardiac organoids to model COVID‐19 cytokine storm induced cardiac injuries

ABSTRACT: Human cardiac organoids to model COVID‐19 cytokine storm induced cardiac injuries

PROVIDER: PRJNA1054224 | ENA |

REPOSITORIES: ENA

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Human cardiac organoids to model COVID‐19 cytokine storm induced cardiac injuries

Project description:Acute cardiac injuries occur in 20%–25% of hospitalized COVID‐19 patients. Herein, we demonstrate that human cardiac organoids (hCOs) are a viable platform to model the cardiac injuries caused by COVID‐19 hyperinflammation. As IL‐1β is an upstream cytokine and a core COVID‐19 signature cytokine, it was used to stimulate hCOs to induce the release of a milieu of proinflammatory cytokines that mirror the profile of COVID‐19 cytokine storm. The IL‐1β treated hCOs recapitulated transcriptomic, structural, and functional signatures of COVID‐19 hearts. The comparison of IL‐1β treated hCOs with cardiac tissue from COVID‐19 autopsies illustrated the critical roles of hyper‐inflammation in COVID‐19 cardiac insults and indicated the cardioprotective effects of endothelium. The IL‐1β treated hCOs thus provide a defined and robust model to assess the efficacy and potential side effects of immunomodulatory drugs, as well as the reversibility of COVID‐19 cardiac in- juries at baseline and simulated exercise conditions.

2023-12-20 | GSE250520 | GEO

Discovery of drugs to treat cytokine storm-induced cardiac dysfunction

Project description:SARS-CoV2 infection leads to cardiac injury and dysfunction in 20-30% of hospitalized patients and higher rates of mortality in patients with pre-existing cardiovascular disease. Inflammatory factors released as part of the 'cytokine storm' are thought to play a critical role in cardiac dysfunction in severe COVID-19 patients. Here we use human cardiac organoid technology combined with high sensitivity phosphoproteomics and single nuclei RNA sequencing to identify inflammatory targets inducing cardiac dysfunction. This new pipeline allowed rapid progress and identification of putative therapeutics. We identify a novel interferon-gamma driven BRD4 (bromodomain protein 4)-fibrosis/iNOS axis as a key intracellular mediator of inflammation-induced cardiac dysfunction. This axis is therapeutically targetable using BRD4 inhibitors, which promoted full recovery of function in human cardiac organoids and prevented severe inflammation and death in a cytokine-storm mouse model. The BRD inhibitor INCB054329 was the most efficacious, and is a prime candidate for drug repurposing to attenuate cardiac dysfunction and improve COVID-19 mortality in humans.

2022-02-21 | PXD020994 | Pride

Persistent viral activity, cytokine storm and lung fibrosis in severe COVID-19

Project description:Persistent viral activity, cytokine storm and lung fibrosis in severe COVID-19

| PRJNA630421 | ENA

sn-RNAseq of cytokine storm in human cardiac organoids

Project description:sn-RNAseq profiling of the impact of a cytokine storm model in human cardiac organoids

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Lethal Cytokine Storm Post-mRNA Booster Vaccination

Project description:Lethal Cytokine Storm Post-mRNA Booster Vaccination

| PRJNA1008117 | ENA

Human Cardiac Organoids to Model COVID-19 Cytokine Storm Induced Cardiac Injuries.

Project description: Not available

| S-EPMC8820666 | biostudies-literature

Human cardiac organoids to model COVID-19 cytokine storm induced cardiac injuries.

Project description: Not available

| S-EPMC9350263 | biostudies-literature

SPLEVs, a new therapeutic modality for cytokine storm syndromes

Project description:Since cytokine storm syndromes such as sepsis, acute respiratory distress syndrome (ARDS) and coagulopathy, including those seen in COVID-19, are fatal, development of highly effective therapeutics is urgently needed. We previously reported that the hydrolysis of extracellular vesicles (EVs) by secreted phospholipase A2 (sPLA2) leads to production of immunomodulatory lipid mediators in lymphoproliferative diseases. We aimed to apply this phenomenon technically using sPLA2-reacted EVs — here in designated as “SPLEVs”, which showed high therapeutic efficacies against various disease. Mechanistically, SPLEVs bind to type II alveolar epithelial cells and elicit “lipid counterstorm”, drastically increasing the production of tissue-protective and anti-inflammatory lipid mediators through the phosphoinositide 3-kinase and sterol regulatory element-binding protein 1 pathways. And these effects showed an important role of PG in hep-EVs, and Lyso-PG hydrolyzed by sPLA2 was involved in the regulation of inflammation. Also, hep-SPLEVs injection showed increased lipid mediators and anti-inflammatory effects in inflammatory diseases other than ARDS, prolonged survival and reduced tissue damage. Thus, SPLEVs are expected to be an effective therapeutic tool for treatment of broad ranges of inflammatory diseases including COVID-19 and other new pandemic diseases.

2026-08-06 | GSE294641 | GEO

SPLEVs, a new therapeutic modality for cytokine storm syndromes

Project description:SPLEVs, a new therapeutic modality for cytokine storm syndromes

| PRJNA1251004 | ENA

An H5N1 virus-encoded atypical microRNA is a major contributor to cytokine storm and mortality

Project description:An H5N1 virus-encoded microRNA directly targets mammalian poly(rC) binding protein 2 and is a major contributor to H5N1-associated ‘cytokine storm’ and mortality.

2017-03-24 | GSE67222 | GEO

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