ArticleJournal of thrombosis and haemostasis : JTH2023
JAK-STAT inhibition reduces endothelial prothrombotic activation and leukocyte-endothelial proadhesive interactions.
Article in Journal of thrombosis and haemostasis : JTH, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
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Who cites it
34 citing papers in PubMed, 46 citations in OpenAlex.
- Review
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- Microfluidic Platforms for Modeling Cancer-Associated Thrombosis: Current Status and Future Directions.Research and practice in thrombosis and haemostasis · 2026Review
- Real-world effectiveness and safety of upadacitinib in Korean patients with inflammatory bowel disease: a single-center retrospective study.Intestinal research · 2026Article
- Endothelial activation and damage associated with steroid-refractory aGVHD are counteracted by ruxolitinib.Blood advances · 2026Article
- Positive and Negative Cardiovascular Effects of JAK Inhibitors in Inflammation.ACR open rheumatology · 2026Review
- Real-world safety signals of baricitinib and in silico exploration of a potential mechanism underlying herpes zoster: a multidisciplinary analysis.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Inflammatory Signaling and Endothelial Activation Drive Thrombosis in Hodgkin and Non-Hodgkin Lymphoma.Cells · 2026Article
- ShenQi DiHuang Decoction (SQDHD) Ameliorates Neuroinflammation and Neuropsychiatric Manifestations in Pristane Induced Lupus Mice via Blocking JAK1-STAT3 Pathway.CNS neuroscience & therapeutics · 2026Article
- Megakaryocytic Emperipolesis in Acute Myeloid Leukemia with Trisomy 8Turkish journal of haematology : official journal of Turkish Society of Haematology · 2026Article
- The Role of Cellular Senescence and SASP in the Pathogenesis of Atherosclerosis and the Therapeutic Potential of Senolytic Strategies in Cardiovascular Diseases.Biomedicines · 2026Review
- JAK inhibitors and adverse cardiovascular events: Class effect or molecule-specific risk?Frontiers in pharmacology · 2026Review
- Guanxinjing ameliorates coronary microvascular dysfunction in myocardial ischemia-reperfusion injury by alleviating inflammation and restoring endothelial function.Frontiers in immunology · 2026Article
- Venous Thromboembolism Risk in Patients with Atopic Dermatitis Treated with Abrocitinib: A Review of Female Patients on Oral Contraception and Nicotine Exposure From the JADE Clinical Trial Program.The Journal of clinical and aesthetic dermatology · 2026Article
- Pathological mechanisms and clinical research progress of endothelial dysfunction.Frontiers in cardiovascular medicine · 2026Review
- The protective effect and mechanism of rhIFN-α1b on lung injury in mice infected with H1N1 influenza A virus.Archives of microbiology · 2025Article
- Clinical and Molecular Insights of Arterial and Venous Thrombosis in Myeloproliferative Diseases-Case-Based Narrative Review.Biomedicines · 2025Review
- Targeting synergetic endothelial inflammation by inhibiting NFKB and JAK-STAT pathways.iScience · 2025Article
- Matrix Metalloproteinases Family Gene Polymorphisms Are Associated with Thrombosis Risk in Myeloproliferative Neoplasms.International journal of molecular sciences · 2025Article
- Effective Treatment of Livedoid Vasculopathy With Oral Tofacitinib.Clinical case reports · 2025Article
Corrections and comments
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundVascular activation is characterized by increased proinflammatory, pro thrombotic, and proadhesive signaling. Several chronic and acute conditions, including Bcr-abl-negative myeloproliferative neoplasms (MPNs), graft-vs-host disease, and COVID-19 have been noted to have increased activation of the janus kinase (JAK)-signal transducer and downstream activator of transcription (STAT) pathways. Two notable inhibitors of the JAK-STAT pathway are ruxolitinib (JAK1/2 inhibitor) and fedratinib (JAK2 inhibitor), which are currently used to treat MPN patients. However, in some conditions, it has been noted that JAK inhibitors can increase the risk of thromboembolic complications.
objectivesWe sought to define the anti-inflammatory and antithrombotic effects of JAK-STAT inhibitors in vascular endothelial cells.
methodsWe assessed endothelial activation in the presence or absence of ruxolitinib or fedratinib by using immunoblots, immunofluorescence, qRT-PCR, and function coagulation assays. Finally, we used endothelialized microfluidics perfused with blood from normal and JAK2
resultsWe found that both ruxolitinib and fedratinib reduced endothelial cell phospho-STAT1 and STAT3 signaling and attenuated nuclear phospho-NK-κB and phospho-c-Jun localization. JAK-STAT inhibition also limited secretion of proadhesive and procoagulant P-selectin and von Willebrand factor and proinflammatory IL-6. Likewise, we found that JAK-STAT inhibition reduced endothelial tissue factor and urokinase plasminogen activator expression and activity.
conclusionsBy using endothelialized microfluidics perfused with whole blood samples, we demonstrated that endothelial treatment with JAK-STAT inhibitors prevented rolling of both healthy control and JAK2
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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.