ArticleLeukemia2014
Ruxolitinib leads to improvement of pulmonary hypertension in patients with myelofibrosis.
Article in Leukemia, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 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.
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.
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Who cites it
42 citing papers in PubMed, 70 citations in OpenAlex.
- The New Era of Pulmonary Hypertension: The Dawn of Disease Modification & Therapeutic Modalities.Journal of cardiovascular development and disease · 2026Review
- Mesenchymal stromal cells alleviate pulmonary arterial hypertension by suppressing pulmonary arterial adventitial fibroblast activation and extracellular matrix remodeling via the SOCS3/STAT3 pathway.Stem cell research & therapy · 2026Article
- Longitudinal prospective analysis of organ stiffness and cardiac function in patients with myelofibrosis treated with ruxolitinib type of study: Prospective single-center cohort study.Therapeutic advances in hematology · 2026Article
- Pulmonary manifestations during neutrophil engraftment in recipients of allogeneic hematopoietic cell transplantation for myelofibrosis.Bone marrow transplantation · 2025Article
- Beyond Thrombosis: Pulmonary Hypertension and Heart Failure in Patients With Myeloproliferative Neoplasms: JACC: CardioOncology State-of-the-Art Review.JACC. CardioOncology · 2025Review
- Relapse of Acute Myelogenous Leukemia With History of Myeloproliferative Neoplasm and Exacerbation of Pulmonary Hypertension.JACC. Case reports · 2025Article
- Therapeutic targets for pulmonary arterial hypertension: insights into the emerging landscape.Expert opinion on therapeutic targets · 2025Review
- Navigating 'grey areas' and challenges during evaluation of transplant eligibility in specific myelofibrosis populations: a perspective on behalf of the Chronic Malignancies Working Party of the EBMT.Bone marrow transplantation · 2025Review
- Integrative Multiomics in the Lung Reveals a Protective Role of Asporin in Pulmonary Arterial Hypertension.Circulation · 2024Article
- Immunotherapy for Pulmonary Arterial Hypertension: From the Pathogenesis to Clinical Management.International journal of molecular sciences · 2024Review
- Cancer Therapy-Associated Pulmonary Hypertension and Right Ventricular Dysfunction: Etiologies and Prognostic Implications.Reviews in cardiovascular medicine · 2024Review
- Ten years of treatment with ruxolitinib for myelofibrosis: a review of safety.Journal of hematology & oncology · 2023Review
- Combination Therapy With Pulmonary Vasodilatation and JAK2 Inhibition for Pulmonary Hypertension With Polycythemia Vera.CJC open · 2023Article
- Innovative strategies to improve hematopoietic stem cell transplant outcomes in myelofibrosis.American journal of hematology · 2022Review
- The role of JAK inhibitors in hematopoietic cell transplantation.Bone marrow transplantation · 2022Review
- Case of Pulmonary Extramedullary Hematopoiesis Responding to Ruxolitinib.Leukemia research reports · 2022Article
- Clonal hematopoiesis with JAK2V617F promotes pulmonary hypertension with ALK1 upregulation in lung neutrophils.Nature communications · 2021Article
- Polycythemia Vera Associated with Pulmonary Hypertension and Diffuse Large B-Cell Lymphoma: A Case Report.The American journal of case reports · 2021Article
- Article
- The Role of JAK/STAT Molecular Pathway in Vascular Remodeling Associated with Pulmonary Hypertension.International journal of molecular sciences · 2021Review
Corrections and comments
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Authors and funding
13 authors at 3 institutions in 1 country.
Funding
Abstract
Pulmonary hypertension (PH) is a frequently under recognized complication of myelofibrosis (MF). The pathophysiology of PH in MF is unknown and no definitive therapies have been established. We studied 15 patients with MF-associated PH and compared their echocardiographic and PH relevant biomarkers (nitric oxide (NO), N-terminal pro-hormone of brain natriuretic peptide (NT-pro BNP), von Willebrand antigen (vWB), ristocetin-cofactor activity (RCA) and uric acid (UA)) pre- and post-ruxolitinib treatment. Ruxolitinib decreased the plasma levels of NT-pro BNP (73%; P=0.043), UA (60%), vWB (86%) and RCA (73%; P=0.036). Improvements in echocardiographic findings were also seen in 66% of patients (P=0.022). Furthermore, marked increase in NO compared with baseline (69.75 vs 40.1 picomolar (pM); P=0.001) was observed post-ruxolitinib therapy, whereas no changes were noted with conventional therapies. Treatment with ruxolitinib also resulted in the reduction of key cytokines (tumor necrosis factor alpha, interleukin-4 (IL-4), IL-6 and IL-8) and induction of interferon-gamma. Animal studies further supported the role of ruxolitinib in the induction of NO levels. In conclusion, aberrant Janus kinase (JAK)-signal transducer and activator of transcription signaling in MF may mediate PH through dysregulation of NO and cytokine levels, which can be restored by therapy with JAK inhibitors suggesting that inhibition of this pathway is a novel target for the management of patients with PH.
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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.