ReviewFrontiers in immunology2023
Chemokines, molecular drivers of thromboinflammation and immunothrombosis.
Review in Frontiers in immunology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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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.
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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.
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Who cites it
26 citing papers in PubMed, 24 citations in OpenAlex.
- Evolution of neutrophil extracellular traps in the pathology of stroke.Neural regeneration research · 2026Article
- Spatiotemporal heterogeneity of neutrophil extracellular traps in hepatocellular carcinoma microenvironment and targeted therapy progress.Journal of translational medicine · 2026Review
- The MCP-1/CCR2-CD16⁺ monocyte axis drives thrombus fibrosis in Chronic Thromboembolic Pulmonary Hypertension.Journal of translational medicine · 2026Article
- Unique molecular profiling of monocyte responses to a high dose of DENV-NS1 reflected the effect of NS1 on hemostasis.Medical microbiology and immunology · 2026Article
- Post-treatment with H12-(ADP)-liposomes after LPS challenge ameliorated coagulopathy and critical organ injury in rats.Intensive care medicine experimental · 2026Article
- Modulation of Chemokine Activity for Enhanced Angiogenesis and Tissue Regeneration in Chronic Wounds.International journal of molecular sciences · 2026Review
- Arterial Thrombosis in Severe Ulcerative Colitis: A Case-Based Narrative Review of Current Evidence.Biomedicines · 2026Review
- GATA4-overexpressing BMSCs-derived exosome regulation of myocardial infarction in mice by key miRNA and apoptosis gene CLU.European journal of medical research · 2026Article
- Machine learning integration of bulk and single-cell RNA-Seq data reveals COPS2 as a central immune regulator in deep vein thrombosis.American journal of translational research · 2026Article
- Elevated neutrophil-to-lymphocyte ratio and platelet-to-lymphocyte ratio in peripheral blood are associated with higher risk of atherosclerotic renal artery stenosis.Frontiers in cardiovascular medicine · 2026Article
- Bridging worlds: a narrative review of IL-17 at the crossroads of inflammation and thrombosis.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2025Review
- Immunothrombosis in Sepsis: Cellular Crosstalk, Molecular Triggers, and Therapeutic Opportunities-A Review.International journal of molecular sciences · 2025Review
- Upregulation of TLR-MYD88 signaling, stem cell genes, and Klotho mediates sepsis-associated myocardial inflammation.Molecular biology reports · 2025Article
- Article
- Platelets and diseases: signal transduction and advances in targeted therapy.Signal transduction and targeted therapy · 2025Review
- Adenovirus vectors can infect mouse megakaryocytes - implications for vaccine-induced thrombosis/thrombocytopenia.Research and practice in thrombosis and haemostasis · 2025Article
- ACKR3 agonism induces heterodimerization with chemokine receptor CXCR4 and attenuates platelet function.European journal of clinical investigation · 2025Article
- Encompassing view of spatial and single-cell RNA sequencing renews the role of the microvasculature in human atherosclerosis.Nature cardiovascular research · 2025Article
- Immunomodulation and Thrombolytic Approaches in the Management of Deep Vein Thrombosis and Pulmonary Embolism.Cardiology and cardiovascular medicine · 2025Article
- Construction of a nomogram for preoperative deep vein thrombosis in pelvic fracture patients.BMC surgery · 2024Article
Corrections and comments
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Authors and funding
2 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Blood clotting is a finely regulated process that is essential for hemostasis. However, when dysregulated or spontaneous, it promotes thrombotic disorders. The fact that these are triggered, accompanied and amplified by inflammation is reflected in the term thromboinflammation that includes chemokines. The role of chemokines in thrombosis is therefore illuminated from a cellular perspective, where endothelial cells, platelets, red blood cells, and leukocytes may be both the source and target of chemokines. Chemokine-dependent prothrombotic processes may thereby occur independently of chemokine receptors or be mediated by chemokine receptors, although the binding and activation of classical G protein-coupled receptors and their signaling pathways differ from those of atypical chemokine receptors, which do not function via cell activation and recruitment. Regardless of binding to their receptors, chemokines can induce thrombosis by forming platelet-activating immune complexes with heparin or other polyanions that are pathognomonic for HIT and VITT. In addition, chemokines can bind to NETs and alter their structure. They also change the electrical charge of the cell surface of platelets and interact with coagulation factors, thereby modulating the balance of fibrinolysis and coagulation. Moreover, CXCL12 activates CXCR4 on platelets independently of classical migratory chemokine activity and causes aggregation and thrombosis via the PI3Kβ and Btk signaling pathways. In contrast, typical chemokine-chemokine receptor interactions are involved in the processes that contribute to the adhesiveness of the endothelium in the initial phase of venous thrombosis, where neutrophils and monocytes subsequently accumulate in massive numbers. Later, the reorganization and resolution of a thrombus require coordinated cell migration and invasion of the thrombus, and, as such, indeed, chemokines recruit leukocytes to existing thrombi. Therefore, chemokines contribute in many independent ways to thrombosis.
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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.