Connecting Transcriptional and Functional Macrophage Heterogeneity in Atherosclerosis.

Connecting Transcriptional and Functional Macrophage Heterogeneity in Atherosclerosis.
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连接动脉粥样硬化中的转录和功能巨噬细胞异质性

DOI:
10.1161/circresaha.119.316168
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发表时间:
2019
影响因子:
20.1
通讯作者:
Koelwyn
Koelwyn
中科院分区:
医学1区
文献类型:
--
作者:
Schlegel;Koelwyn

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相似文献

巨噬细胞在动脉壁中的积聚是动脉粥样硬化的标志,并且这些免疫细胞在动脉粥样硬化斑块的起始、进展和最终破裂中起关键作用。1斑块巨噬细胞有各种来源:它们可以被招募到组织中,2可以在胚胎植入后增殖,3甚至可以来源于转分化的平滑肌细胞。4此外,体外成像已经建立了不同类型的单核细胞和巨噬细胞向病变部位的阶段依赖性募集。[5]毫不奇怪,新兴的单细胞技术揭示了斑块巨噬细胞库是非常异质的,包含大量转录上不同的亚群。6-8将这种转录异质性与功能表型和体内细胞行为联系起来是理解巨噬细胞动力学在动脉粥样硬化发病机制中作用的新挑战。
Macrophage accumulation in the artery wall is a hallmark of atherosclerosis, and these immune cells play key roles in the initiation, progression, and eventual rupture of atherosclerotic plaques. 1 Plaque macrophages have various origins: they can be recruited into the tissue, 2 can proliferate after being embryonically implanted, 3 or can even derive from transdifferentiated smooth muscle cells. 4 Moreover, in vitro imaging has established stage-dependent recruitment of different types of monocytes and macrophages into the lesion site. 5 Not surprisingly, emerging single-cell technologies have unveiled that the plaque macrophage pool is vastly heterogeneous, containing a plethora of transcriptionally distinct subpopulations. 6–8 Connecting this transcriptional heterogeneity to functional phenotypes and in vivo cell behavior is a new challenge in understanding the role of macrophage dynamics in the pathogenesis of atherosclerosis.
DOI: 10.1172/jci.insight.124574
发表时间: 2019-02-21
期刊: JCI INSIGHT
影响因子: 8
作者:
Lin, Jian-Da;Nishi, Hitoo;Loke, P'ng
通讯作者: Loke, P'ng
DOI: 10.1161/circresaha.119.315175
发表时间: 2019-12-06
影响因子: 20.1
作者:
McArdle, Sara;Buscher, Konrad;Ley, Klaus
通讯作者: Ley, Klaus
DOI: 10.1161/circresaha.117.312513
发表时间: 2018-06-08
影响因子: 20.1
作者:
Winkels H;Ehinger E;Vassallo M;Buscher K;Dinh HQ;Kobiyama K;Hamers AAJ;Cochain C;Vafadarnejad E;Saliba AE;Zernecke A;Pramod AB;Ghosh AK;Anto Michel N;Hoppe N;Hilgendorf I;Zirlik A;Hedrick CC;Ley K;Wolf D
通讯作者: Wolf D