Discover Community Create You

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

Bystander effect of SARS-CoV-2 spike protein on human monocytic THP-1 cell activation and initiation of prothrombogenic stimulus representing severe COVID-19

30 Dec 2022

Abstract excerpt

BACKGROUND: Hypercoagulable state and thromboembolic complications are potential life-threatening events in COVID-19 patients. Our previous studies demonstrated that SARS-CoV-2 infection as well as viral spike protein expressed epithelial cells exhibit senescence with the release of inflammatory molecules, including alarmins. FINDINGS: We observed extracellular alarmins present in the culture media of SARS-CoV-2...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to Complement system in diseases
Share to COVID-19 Clinical Research Studies
Share to SARS-CoV-2 and COVID-19 Research

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Source

Identifiers

PMID: 36585712
DOI: 10.1186/s12950-022-00325-8

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Bystander effect of SARS-CoV-2 spike protein on human monocytic THP-1 cell activation and initiation of prothrombogenic stimulus representing severe COVID-19PMID 36585712Read ↗

SARS-CoV-2 spike protein expressing epithelial cells promotes senescence associated secretory phenotype in endothelial cells and increased inflammatory responseSemantic proximity Read ↗

COVID-19: role of the NLRP3 inflammasomeSemantic proximity Read ↗

SARS-CoV-2 spike protein activates NOX2-p66SHC axis via inhibiting SLAMF8 to promote thrombogenesisSemantic proximity Read ↗

Sustained vascular inflammatory effects of SARS-CoV-2 spike protein on human endothelial cellsSemantic proximity Read ↗

SARS-CoV-2 Spike protein activates TMEM16F-mediated platelet pro-coagulant activitySemantic proximity Read ↗

Protein C Pretreatment Protects Endothelial Cells from SARS-CoV-2-Induced ActivationSemantic proximity Read ↗

SARS-CoV-2 enhances complement-mediated endothelial injury via the suppression of membrane complement regulatory proteinsSemantic proximity Read ↗

COVID-19 Sepsis: Pathogenesis and Endothelial Molecular Mechanisms Based on "Two-Path Unifying Theory" of Hemostasis and Endotheliopathy-Associated Vascular Microthrombotic Disease, and Proposed Therapeutic Approach with Antimicrothrombotic Therapy.Semantic proximity Read ↗

Neutrophil extracellular traps and macrophage activation contibute to thrombosis and post-covid syndrome in SARS-CoV-2 infectionSemantic proximity Read ↗

Prothrombotic Phenotype in COVID-19: Focus on Platelets.Semantic proximity Read ↗

Mechanisms of Immunothrombosis by SARS-CoV-2Semantic proximity Read ↗

SARS-CoV-2 Spike protein promotes vWF secretion and thrombosis via endothelial cytoskeleton-associated protein 4 (CKAP4)Semantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.