Endothelial progenitor cells: a promising therapeutic alternative for cardiovascular disease.
Endothelial progenitor cells: a promising therapeutic alternative for cardiovascular disease.
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DOI：
10.1111/j.1540-8183.2007.00251.x
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发表时间：
2007-04-01
影响因子：
2.1
通讯作者：
Goldschmidt-Clermont, Pascal J
中科院分区：
文献类型：
--
作者：
Dong, Chunming;Goldschmidt-Clermont, Pascal J
内皮单层的完整性和功能活性在防止动脉粥样硬化性疾病进展中起着关键作用。动脉粥样硬化危险因素对内皮细胞的损伤可导致内皮细胞凋亡，同时内皮细胞的完整性丧失。因此，修复受损血管以再生内皮细胞为目标的方法已经在临床前实验模型和临床研究中进行了测试。事实上，来自骨髓的内皮祖细胞(EPC)已被证明整合到新生血管的部位和内皮剥脱的部位。这些细胞可能提供内源性修复机制，以对抗持续的危险因素诱导的内皮损伤，并取代功能障碍的内皮细胞。然而，冠状动脉疾病的危险因素，如年龄、吸烟、高血压、高脂血症和糖尿病，会减少循环内皮祖细胞的数量和功能活性，潜在地限制祖细胞的治疗前景和限制再生能力。此外，危险因素对内皮祖细胞的损害可能有助于动脉粥样硬化的形成和疾病的进展。文章综述了内皮祖细胞在动脉粥样硬化形成和预测心血管预后中的作用，并强调了在制定旨在干预损伤和修复机制平衡的治疗策略方面的潜在挑战。
The integrity and functional activity of the endothelial monolayer play a critical role in preventing atherosclerotic disease progression. Endothelial cell (EC) damage by atherosclerosis risk factors can result in EC apoptosis with loss of the integrity of the endothelium. Thus, approaches to repair the injured vessels with the goal of regenerating ECs have been tested in preclinical experimental models and in clinical studies. Indeed, endothelial progenitor cells (EPCs) originating from the bone marrow have been shown to incorporate into sites of neovascularization and home to sites of endothelial denudation. These cells may provide an endogenous repair mechanism to counteract ongoing risk factor-induced endothelial injury and to replace dysfunctional endothelium. Risk factors for coronary artery disease, such as age, smoking, hypertension, hyperlipidemia, and diabetes, however, reduce the number and functional activity of circulating EPCs, potentially restricting the therapeutic prospective of progenitor cells and limiting the regenerative capacity. Furthermore, the impairment of EPCs by risk factors may contribute to atherogenesis and atherosclerotic disease progression. The article reviews the role of EPCs in atherogenesis and in predicting cardiovascular outcomes, and highlights the potential challenges in developing therapeutic strategies aiming to interfere with the balance of injury and repair mechanisms.