SynthesisScientific reports2022
Tissue factor links inflammation, thrombosis, and senescence in COVID-19.
Synthesis in Scientific reports, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers, 1 of them a synthesis that pooled it.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
17 citing papers in PubMed, 1 synthesis or guideline pooled it, 26 citations in OpenAlex.
- Cellular senescence in acute human infectious disease: a systematic review.Frontiers in aging · 2024Pooled it
- Translating animal models of SARS-CoV-2 infection to vascular, neurological and gastrointestinal manifestations of COVID-19.Disease models & mechanisms · 2025Review
- Isostrictiniin Alleviates LPS-Induced Acute Lung Injury via the Regulation of the Keap1-Nrf2/HO-1 and MAPK/NF-κB Signaling Pathways.International journal of molecular sciences · 2025Article
- Neutrophils: Linking Inflammation to Thrombosis and Unlocking New Treatment Horizons.International journal of molecular sciences · 2025Review
- PROS1 released by lung basal cells limits inflammation in epithelial and monocytes during SARS-CoV-2 infection.Discovery immunology · 2025Article
- Assessing the endothelium's role in COVID-19 severity using the HUVEC model.Frontiers in immunology · 2025Article
- SARS-CoV-2 infection of human pluripotent stem cell-derived vascular cells reveals smooth muscle cells as key mediators of vascular pathology during infection.Nature communications · 2024Article
- Review
- Longitudinal analysis of the lung proteome reveals persistent repair months after mild to moderate COVID-19.Cell reports. Medicine · 2024Article
- Women With a History of Preeclampsia Exhibit Accelerated Aging and Unfavorable Profiles of Senescence Markers.Hypertension (Dallas, Tex. : 1979) · 2024Article
- Exploring the Pathophysiology of Long COVID: The Central Role of Low-Grade Inflammation and Multisystem Involvement.International journal of molecular sciences · 2024Review
- Monocyte-Mediated Thrombosis Linked to Circulating Tissue Factor and Immune Paralysis in COVID-19.Arteriosclerosis, thrombosis, and vascular biology · 2024Article
- Multi-Omics Profiling Reveals Phenotypic and Functional Heterogeneity of Neutrophils in COVID-19.International journal of molecular sciences · 2024Article
- Exploring the Mechanism of Chuanxiong Rhizoma against Thrombosis Based on Network Pharmacology, Molecular Docking and Experimental Verification.Molecules (Basel, Switzerland) · 2023Article
- Tissue factor is a critical regulator of radiation therapy-induced glioblastoma remodeling.Cancer cell · 2023Article
- On frailty and accelerated aging during SARS-Cov-2: senescence.Aging clinical and experimental research · 2023Article
- Microvascular Thrombosis as a Critical Factor in Severe COVID-19.International journal of molecular sciences · 2023Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
COVID-19 is a highly contagious respiratory infection caused by the SARS-CoV-2 virus. The infected lung epithelial cells secrete a group of chemokines and cytokines, which triggers harmful cytokine storms and hyper-thrombotic responses. Recent studies have proposed that viral-induced senescence is responsible for cytokine release and inflammation in COVID-19 patients. However, it is unknown whether cellular senescence is commonly triggered after viral infection and how inflammation and thrombosis, hyper-activated in these patients, are functionally connected. To address these questions, we conducted a bioinformatics-based meta-analysis using single-cell and bulk RNA sequencing datasets obtained from human patient studies, animal models, and cell lines infected with SARS-CoV-2 and other respiratory viruses. We found that the senescence phenotype is robustly upregulated in most SARS-CoV-2-infected patients, especially in the infected lung epithelial cells. Notably, the upregulation of Tissue factor (F3), a key initiator of the extrinsic blood coagulation pathway, occurs concurrently with the upregulation of the senescence-associated secretory phenotype (SASP) factors. Furthermore, F3 levels are positively correlated with the senescence and hyper-coagulation gene signatures in COVID-19 patients. Together, these data demonstrate the prevalence of senescence in respiratory viral infection and suggest F3 as a critical link between inflammation, thrombosis, and senescence in these disease states.
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What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.