Deletion of the murine ortholog of human 9p21.3 locus promotes atherosclerosis by increasing macrophage proinflammatory activity.

Sanna Kettunen,Anna-Kaisa Ruotsalainen,Tiit Örd,Tuisku Suoranta,Janne Heikkilä,Minna U Kaikkonen,Nihay Laham-Karam,Seppo Ylä-Herttuala

Frontiers in cardiovascular medicine（2023）

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摘要

These data demonstrate that both systemic and BM-specific deletion of the murine 9p21.3 risk locus ortholog promotes atherosclerosis and regulates macrophage pro-inflammatory activity, suggesting the inflammation-driven mechanisms of the risk locus on atherogenesis.

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关键词

ANRIL,Chr9p21.3,atherosclerosis,coronary artery disease,inflammation,macrophage,mouse model

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