Mischief in the marrow: a root of cardiovascular evil.
Mischief in the marrow: a root of cardiovascular evil.
复制标题
祸根骨髓：心血管之祸根。
DOI：
10.1093/eurheartj/ehac149
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发表时间：
2022
影响因子：
39.3
通讯作者：
Swirski,FilipK
中科院分区：
文献类型：
--
作者：
Libby,Peter;Nahrendorf,Matthias;Swirski,FilipK
骨髓造血增加对心血管疾病的不同驱动因素的反应。在小鼠中进行的大量实验已经证明，测试的几种传统风险因素，包括高血压，高胆固醇血症和高胆固醇血症，可以增加造血（列于右侧）。与心血管疾病相关的骨髓激活的其他刺激包括睡眠碎片和心理社会压力。在人类中验证小鼠中的这些观察结果已经落后。PESA的新发现有助于缩小这一差距，显示左侧列出的代谢综合征的组成部分可以增加骨髓中葡萄糖类似物FDG的摄取，如正电子发射断层扫描成像所确定的。在一个明显健康的人群中，这些关于慢性危险因素的观察结果补充了在经历急性冠状动脉综合征的人中的观察结果，该观察结果显示骨髓和脾脏中的FDG摄取增加。实验和人体观察结果共同为骨髓活化和造血增加可促进动脉粥样硬化的发展这一概念提供了强有力的支持。
Graphical Abstract Bone marrow haematopoiesis increases in response to diverse drivers of cardiovascular disease. Numerous experiments in mice have demonstrated that several traditional risk factors tested, including hypertension, hypercholesterolaemia, and hyperglycaemia, can augment haematopoiesis (listed on the right). Other stimuli to bone marrow activation relevant to cardiovascular disease include sleep fragmentation and psychosocial stress. The validation in humans of these observations in mice has lagged behind. The new findings from PESA help to close this gap by showing that the components of the metabolic syndrome listed on the left can increase glucose analogue FDG uptake in bone marrow as determined by positron emission tomographic imaging. These observations on chronic risk factors, in an apparently well population, complement observations in humans undergoing acute coronary syndrome that show increased FDG uptake in both the bone marrow and the spleen. The experimental and human observations together provide strong support for the concept that bone marrow activation and increased haematopoiesis can contribute to the development of atherosclerosis.