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Cardiovascular Events: A Challenge in JAK2-positive Myeloproliferative Neoplasms
Habib Haybar1, Elahe Khodadi2, Mohammad Shahjahani3
1Atherosclerosis Research Center, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran.
Insights
The JAK2V617F mutation in myeloproliferative neoplasms (MPNs) increases cardiovascular event risk. Identifying this mutation aids diagnosis and prevention of heart complications in MPN patients.
Area of Science:
- Hematology
- Cardiology
- Molecular Biology
Background:
- Myeloproliferative neoplasms (MPNs) are chronic blood disorders characterized by myeloid lineage clonal expansion.
- Essential thrombocythemia (ET), polycythemia vera (PV), primary myelofibrosis (PMF), and chronic myeloid leukemia (CML) are key MPNs.
- Cardiovascular events pose a significant mortality risk for MPN patients.
Purpose of the Study:
- To review cardiovascular events in patients with JAK2-positive myeloproliferative neoplasms.
- To explore the role of the JAK2V617F mutation in MPN-related cardiovascular complications.
- To discuss the implications of JAK/STAT signaling in MPN cardiotoxicity.
Main Methods:
- A literature search was conducted on PubMed for articles published between 1995 and 2017.
- Keywords included "Cardiovascular Events", "JAK2", and "Myeloproliferative Neoplasms".
- Forty-three relevant articles were selected for review.
Main Results:
- JAK2V617F mutation is prevalent in Philadelphia-negative MPNs like ET and PV, elevating cardiovascular risk.
- JAK2 mutations impact cardiac arteries and veins, leading to thrombosis and ischemia.
- JAK2 phosphorylates STAT proteins, influencing gene expression and contributing to cardiovascular complications via autocrine mechanisms.
Conclusions:
- JAK2 mutation presence correlates with thrombosis and ischemia, aiding cardiovascular event diagnosis even without a clear MPN diagnosis.
- Targeting the JAK/STAT signaling pathway offers a potential strategy for preventing cardiovascular complications in MPN patients.
- Early identification of JAK2 mutations is crucial for managing cardiovascular risks in MPN.
Background:
Myeloproliferative neoplasms (MPNs) are chronic blood disorders caused by clonal expansion in one or more myeloid lineages and include essential thrombocythemia (ET), polycythemia vera (PV), primary myelofibrosis (PMF) and chronic myeloid leukemia (CML). Cardiovascular events are a main challenge for patients with MPN and can lead to their death.
Objective:
JAK2V617F mutation is observed in Philadelphia-negative MPNs such as ET and PV, increasing the risk of cardiovascular complications in these patients. JAK2 mutation can affect cardiac arteries and veins in ET and PV, which results in thrombosis, ischemia and other cardiovascular events. JAK/STAT signaling pathway plays an important role in heart diseases. In this review, we will survey the cardiovascular events in JAK2-positive MPN patients.
Method:
Relevant English-language literature were searched and retrieved from PubMed search engine (1995-2017). The following keywords were used: "Cardiovascular Events", "JAK2" and "Myeloproliferative Neoplasms". Forty three articles were selected by using the key words.
Results:
JAK2 phosphorylates the signal transducers and activators of transcription (STAT). Various factors like angiotensin II (ANG II) and cardiotrophin-1 (CT-1) can bind their receptors on myocytes and increase the expression of angiotensinogen (Ao) gene by binding of STAT proteins to these factors in myocytes, causing different cardiovascular complications through autocrine mechanisms.
Conclusion:
JAK2 mutation is observed in patients with thrombosis, ischemia and other cardiovascular complications having abnormal increase in cell count even without definite clinical diagnosis of MPN. Therefore, identification of this mutation in these patients contributes to definite diagnosis of cardiovascular events. Also, cardiovascular complications in MPN patients can be prevented by targeting the factors involved in JAK/STAT signaling pathway.
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