ArticleJournal of hematology & oncology2014
Cardiac hypertrophy associated with myeloproliferative neoplasms in JAK2V617F transgenic mice.
Article in Journal of hematology & oncology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 29 citations in OpenAlex.
- The Potential Protective Effects of Resveratrol Against Cabazitaxel-Induced Oxidative Stress and Cardiotoxicity in Rats.Cardiovascular toxicology · 2026Article
- Intersecting Pathways: The Impact of Philadelphia-Negative Chronic Myeloproliferative Neoplasms on the Pathogenesis and Progression of Heart Failure with Preserved Ejection Fraction.Diagnostics (Basel, Switzerland) · 2025Article
- Cardiac hypertrophy in polycythemia vera: A case report and review of literature.World journal of cardiology · 2024Article
- Adipose Stem Cell-Seeded Decellularized Porcine Pericardium: A Promising Functional Biomaterial to Synergistically Restore the Cardiac Functions Post-Myocardial Infarction.Veterinary sciences · 2023Article
- Effect of trehalose on heart functions in rats model after myocardial infarction: assessment of novel intraventricular pressure and heart rate variability.Frontiers in cardiovascular medicine · 2023Article
- A One-Stop Protocol to Assess Myocardial Fibrosis in Frozen and Paraffin Sections.Methods and protocols · 2022Article
- Changes in Cardiac Function During the Development of Uremic Cardiomyopathy and the Effect of Salvianolic Acid B Administration in a Rat Model.Frontiers in veterinary science · 2022Article
- Pathogenesis of cardiovascular events in BCR-ABL1-negative myeloproliferative neoplasms.Leukemia · 2021Review
- Endothelial JAK2V617F mutation leads to thrombosis, vasculopathy, and cardiomyopathy in a murine model of myeloproliferative neoplasm.Journal of thrombosis and haemostasis : JTH · 2020Article
- The role of clonal haematopoiesis in cardiovascular diseases: epidemiology and experimental studies.Journal of internal medicine · 2020Review
- Clonal Hematopoiesis: A New Step Linking Inflammation to Heart Failure.JACC. Basic to translational science · 2020Review
- miR-543 regulates the epigenetic landscape of myelofibrosis by targeting TET1 and TET2.JCI insight · 2020Article
- HDAC11 deficiency disrupts oncogene-induced hematopoiesis in myeloproliferative neoplasms.Blood · 2020Article
- Incremental Utility of Right Ventricular Dysfunction in Patients With Myeloproliferative Neoplasm-Associated Pulmonary Hypertension.Journal of the American Society of Echocardiography : official publication of the American Society of Echocardiography · 2019Article
- Article
- JAK2 mutation and acute coronary syndrome complicated with stent thrombosis.Heart and vessels · 2016Article
- P-selectin-mediated LOX expression promotes insulinoma growth in Rip1-Tag2 mice by increasing tissue stiffness.International journal of biological sciences · 2016Article
- Quantitative analyses of myelofibrosis by determining hydroxyproline.Stem cell investigation · 2015Article
- Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 2 countries.
Funding
Abstract
backgroundMyeloproliferative neoplasms (MPNs) are blood malignancies manifested in increased production of red blood cells, white blood cells, and/or platelets. A major molecular lesion associated with the diseases is JAK2V617F, an activation mutation form of tyrosine kinase JAK2. Cardiovascular events represent the leading cause of morbidity and mortality associated MPNs, but the underlying mechanism is not well understood.
methodsPreviously, we generated JAK2V617F transgenic mice which displayed MPN-like phenotypes. In the present study, we further characterized these mice by analyzing the time course of MPN phenotype development and associated cardiac abnormalities. We performed detailed histochemical staining of cardiac sections.
resultsJAK2V617F transgenic mice developed cardiomegaly as a subsequent event of increased blood cell production during the course of MPN phenotype development. The cardiomegaly is manifested in increased ventricular wall thickness and enlarged cardiomyocytes. Trichrome and reticulin staining revealed extensive collagen fibrosis in the heart of JAK2V617F transgenic mice. Thrombosis in the coronary artery and inflammatory cell infiltration into cardiac muscle were also observed in JAK2V617F transgenic mice, and the latter event was accompanied by fibrosis.
conclusionJAK2V617F-induced blood disorders have a major impact on heart function and lead to cardiac hypertrophy. JAK2V617F transgenic mice represent an excellent model system to study both hematological malignancies and cardiovascular diseases.
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