Nov 12, 2019

JAK2V617F -Mediated Clonal Hematopoiesis Accelerates Pathological Remodeling in Murine Heart Failure

JACC. Basic to Translational Science
Soichi SanoKenneth Walsh

Abstract

Janus kinase 2 (valine to phenylalanine at residue 617) (JAK2 V617F ) mutations lead to myeloproliferative neoplasms associated with elevated myeloid, erythroid, and megakaryocytic cells. Alternatively these same mutations can lead to the condition of clonal hematopoiesis with no impact on blood cell counts. Here, a model of myeloid-restricted JAK2 V617F expression from lineage-negative bone marrow cells was developed and evaluated. This model displayed greater cardiac inflammation and dysfunction following permanent left anterior descending artery ligation and transverse aortic constriction. These data suggest that JAK2 V617F mutations arising in myeloid progenitor cells may contribute to cardiovascular disease by promoting the proinflammatory properties of circulating myeloid cells.

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Mentioned in this Paper

JAK2 protein, human
Enhancer-binding protein NF-E4
Aorta Constriction
Cardiovascular Diseases
Clone
Blood Cell Count
Inflammation
Anterior Descending Branch of Left Coronary Artery
Pathologic Processes
JAK2 gene

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