Endothelial progenitor cells in vascular repair and remodeling
Endothelial progenitor cells in vascular repair and remodeling
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DOI：
10.1016/j.phrs.2008.07.008
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发表时间：
2008-08-01
影响因子：
9.3
通讯作者：
Weber, Christian
中科院分区：
文献类型：
--
作者：
Hristov, Mihail;Weber, Christian
出生后的骨髓含有一种独特的祖细胞亚型，具有分化为功能性内皮细胞的能力。因此，这些细胞被称为内皮祖细胞（EPCs）。一般来说，循环EPCs的特征在于CD 133、CD 34和血管内皮生长因子受体2（VEGFR 2）的表达。最近的数据还描述了一些CD 14（+/低）髓系亚群作为功能性内皮前体。令人信服的证据在体内已经进一步出现，血管归巢内皮祖细胞有助于内皮再生，从而限制动脉损伤后的新生内膜增生。然而，在原发性动脉粥样硬化的背景下，斑块进展和不稳定，注射EPCs以及应用干细胞动员因子已被证明与转化为不稳定斑块表型相关。临床上，EPCs的数量和功能与内皮功能或再生的改善呈正相关，但通常与心血管风险（因素）呈负相关。因此，考虑到内皮祖细胞在原发性动脉粥样硬化与动脉损伤的血管修复和重塑中的双重作用，并确定选择性控制其募集的机制，对于改善预测和直接调节内源性血管稳态至关重要。(c)2008爱思唯尔有限公司保留所有权利。
Postnatal bone marrow contains a subtype of unique progenitor cells that have the capacity to differentiate into functional endothelial cells. Hence, these cells have been termed endothelial progenitor cells (EPCs). In general, circulating EPCs were characterized by the expression of CD133, CD34 and the vascular endothelial growth factor receptor-2 (VEGFR2). Recent data have additionally described some CD14(+/low) myeloid subsets as functional endothelial precursors. Convincing evidence in vivo has further emerged that the vascular homing of EPCs contributes to endothelial regeneration thereby limiting neointimal hyperplasia after arterial injury. However, in the context of primary atherosclerosis, plaque progression and destabilization, injection of EPCs as well as application of stem-cell mobilizing factors have been shown to correlate with conversion to unstable plaque phenotype. Clinically, the number and function of EPCs have been positively linked with an improved endothelial function or regeneration but frequently inversely correlated with cardiovascular risk (factors). Thus, considering the dual contribution of EPCs in vascular repair and remodeling in primary atherosclerosis versus arterial injury and identifying mechanisms for selective control of their recruitment appears crucial to improve prediction and to directly modulate endogenous vascular homeostasis. (c) 2008 Elsevier Ltd. All rights reserved.