ReviewCurrent drug targets2022
Fibrinogen, Fibrin, and Fibrin Degradation Products in COVID-19.
Review in Current drug targets, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
31 citing papers in PubMed, 42 citations in OpenAlex.
- Glycine by enteral route does not improve major clinical outcomes in severe COVID-19: a randomized clinical pilot trial.Scientific reports · 2024Trial
- mGem: Population genomics ofmBio · 2026Article
- Observational
- SARS-CoV-2 spike protein can bind fibrin(ogen), but does not alter plasma fibrin formation, clot structure, or lysis.Blood advances · 2026Article
- SARS-CoV-2 Effects on Respiratory and Neurological Systems: Morphological Findings and Gene Expression in K18-hACE2 Mice Model.Microorganisms · 2026Article
- Biomarkers of Coagulation Disorders-Where to from Here?Biomolecules · 2026Review
- Genetic determinants of metabolic-inflammatory dysregulation and machine learning prediction of COVID-19.Frontiers in cellular and infection microbiology · 2026Article
- Glycocalyx at the host-virus interface: a double-edged sword in virus infection and tissue damage.Frontiers in molecular biosciences · 2026Review
- Low-dose heparin sodium as a protective factor against bronchiolitis obliterans formation after adenovirus infection.Annals of medicine · 2025Article
- Hematologic and Immunologic Overlap Between COVID-19 and Idiopathic Pulmonary Fibrosis.Journal of clinical medicine · 2025Review
- Review
- Article
- SARS-CoV-2 (MA10) Infection Aggravates Cerebrovascular Pathology in Endothelial Nitric Oxide Synthase-Deficient Mice.Viruses · 2025Article
- Protofibril packing density of individual fibers alters fibrinolysis.Research and practice in thrombosis and haemostasis · 2025Article
- Deconstructing fibrin(ogen) structure.Journal of thrombosis and haemostasis : JTH · 2025Review
- Immune dysregulation and endothelial dysfunction associate with a pro-thrombotic profile in Long COVID.Frontiers in immunology · 2025Article
- IgA autoimmunity and coagulation among post-acute sequelae of SARS-CoV-2 infection (PASC) patients with persistent respiratory symptoms: a case-control study.Frontiers in immunology · 2025Article
- Proteomic signatures of vaccine-induced and breakthrough infection-induced host responses to SARS-CoV-2.Vaccine · 2025Article
- Thromboinflammation vs. immunothrombosis: strategies for overcoming anticoagulant resistance in COVID-19 and other hyperinflammatory diseases. Is ROTEM helpful or not?Frontiers in immunology · 2025Review
- Article
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
Severe Acute Respiratory Syndrome Coronavirus-2 (SARS-CoV-2) is the highly pathogenic and highly transmissible human coronavirus that is the causative agent for the worldwide COVID-19 pandemic. COVID-19 manifests predominantly as a respiratory illness with symptoms consistent with viral pneumonia, but other organ systems (e.g., kidney, heart, brain) can also become perturbed in COVID-19 patients. Accumulating data suggest that significant activation of the hemostatic system is a common pathological manifestation of SARS-CoV-2 infection. The clotting protein fibrinogen is one of the most abundant plasma proteins. Following activation of coagulation, the central coagulation protease thrombin converts fibrinogen to fibrin monomers, which selfassemble to form a matrix, the primary structural component of the blood clot. Severe COVID-19 is associated with a profound perturbation of circulating fibrinogen, intra- and extravascular fibrin deposition and persistence, and fibrin degradation. Current findings suggest high levels of fibrinogen and the fibrin degradation product D-dimer are biomarkers of poor prognosis in COVID-19. Moreover, emerging studies with in vitro and animal models indicate fibrin(ogen) as an active player in COVID-19 pathogenesis. Here, we review the current literature regarding fibrin(ogen) and COVID-19, including possible pathogenic mechanisms and treatment strategies centered on clotting and fibrin(ogen) function.
Indexed as
Identifiers
What Socratic 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 Socratic graph.