Endothelial progenitor cells in neovascularization of infarcted myocardium.
Endothelial progenitor cells in neovascularization of infarcted myocardium.
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DOI：
10.1016/j.yjmcc.2008.08.003
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发表时间：
2008-10
影响因子：
5
通讯作者：
Losordo, Douglas W.
中科院分区：
文献类型：
--
作者：
Jujo, Kentaro;Ii, Masaaki;Losordo, Douglas W.
关键词：
历史上，缺血组织的血运重建被认为是通过邻近组织中内皮细胞的迁移和增殖而发生的；然而，近年来积累的证据表明，成体外周血细胞亚群，统称为内皮祖细胞(EPCs1)，可以分化为成熟的内皮细胞。在缺血损伤后，内皮祖细胞被认为是新生血管的所在地，在那里它们通过形成毛细血管的结构成分和分泌血管生成因子来促进血管再生；新的证据表明，内皮祖细胞也可以分化为心肌细胞和平滑肌细胞。这些对组织形成的分子和细胞过程的洞察表明，通过将内皮祖细胞移植到缺血的心脏组织中，心肌梗死后的心脏功能可以得到保护，从而促进血管和心肌的恢复。这种治疗策略在缺血性疾病的动物模型中是有效的，随机临床试验的结果表明，基于细胞的策略可能是安全和可行的，用于治疗人类的心肌梗死，并提供了有效性的早期证据。然而，外周血中内皮祖细胞的稀缺以及一些疾病状态减少内皮祖细胞数量和/或功能的证据促使了几种策略的发展，以克服这些限制，例如应用过表达血管生成生长因子的转基因内皮祖细胞。为了优化治疗结果，研究人员必须继续改进EPC的纯化、扩增和给药方法，并开发克服EPC固有的稀缺性和表型缺陷的技术。
Historically, revascularization of ischemic tissue was believed to occur through the migration and proliferation of endothelial cells in nearby tissues; however, evidence accumulated in recent years indicates that a subpopulation of adult, peripheral-blood cells, collectively referred to as endothelial progenitor cells (EPCs1), can differentiate into mature endothelial cells. After ischemic insult, EPCs are believed to home to sites of neovascularization, where they contribute to vascular regeneration by forming a structural component of capillaries and by secreting angiogenic factors; new evidence indicates that EPCs can also differentiate into cardiomyocytes and smooth-muscle cells. These insights into the molecular and cellular processes of tissue formation suggest that cardiac function may be preserved after myocardial infarction by transplanting EPCs into ischemic heart tissue, thereby enhancing vascular and myocardial recovery. This therapeutic strategy has been effective in animal models of ischemic disorders, and results from randomized clinical trials suggest that cell-based strategies may be safe and feasible for treatment of myocardial infarction in humans and have provided early evidence of efficacy. However, the scarcity of EPCs in the peripheral blood and evidence that several disease states reduce EPC number and/or function have prompted the development of several strategies to overcome these limitations, such as the administration of genetically modified EPCs that overexpress angiogenic growth factors. To optimize therapeutic outcomes, researchers must continue to refine methods of EPC purification, expansion, and administration, and to develop techniques that overcome the intrinsic scarcity and phenotypic deficiencies of EPCs.
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