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Editorial
. 2018 Nov 9;123(11):1180-1182.
doi: 10.1161/CIRCRESAHA.118.314074.

Jak-ing Up the Plaque's Lipid Core…and Even More

Peter Libby  1 , Roberto Molinaro  1 , Rob S Sellar  2   3   4 , Benjamin L Ebert  5
Affiliations
Editorial

Jak-ing Up the Plaque's Lipid Core…and Even More

Peter Libby et al. Circ Res. .
No abstract available

Keywords: Editorials; atherosclerosis; bone marrow; inflammation; leukocytes; macrophages.

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Figures

Figure 1A:
Figure 1A:
Clonal Hematopoiesis, as explained in the text, arises from somatic mutations in bone marrow stem cells, associated with ageing, that confer a proliferative advantage on the mutant clone. Mutations in Tet2 and in DNMT3A likely augment expression of pro-inflammatory genes by epigenetic regulation. Jak2 mutation can enhance NET formation, implicated in thrombosis, among other effects shown in B. Modified from reference 4.(Illustration Credit: Ben Smith).
Figure 1B:
Figure 1B:
The JakV617F can influence atherothrombosis both by actions within the plaque and by effects on circulating leukocytes. The left side of this diagram depicts some of the alterations in aspects of plaques demonstrated in mice bearing the JakV617F mutation. Impaired efferocytosis contributes to an enlarged lipid core. Increased erythrocytosis favors deposition of iron derived from heme that can generate the highly oxidant hydroxyl radical augmenting local oxidative stress. Mutant granulocytes in the blood compartment (right side) have a heightened tendency to form NETs, which may favor thrombosis and propagate vascular injury. They also have activation of β1 and β2 integrins, that can enhance attachment to the endothelium, where they may contribute to endothelial damage and thus promote thrombosis. (Illustration Credit: Ben Smith).
See this image and copyright information in PMC

Comment on

References

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