Macrophage Inflammation, Erythrophagocytosis, and Accelerated Atherosclerosis in <i>Jak2</i> ^<i>V617F</i> Mice

Abstract

Hematopoietic Jak2 ^VF expression promotes early lesion formation and increased complexity in advanced atherosclerosis. In addition to increasing hematopoiesis and neutrophil infiltration in early lesions, Jak2 ^VF caused cellular defects in erythrocytes and macrophages, leading to increased erythrophagocytosis but defective efferocytosis. These changes promote accumulation of iron in plaques and increased necrotic core formation which, together with exacerbated proinflammatory responses, likely contribute to plaque instability.