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[内皮祖细胞与动脉粥样硬化]

[Endothelial progenitor cells and atherosclerosis].

作者信息

Hamed Saher, Roguin Ariel

机构信息

Department of Cardiology, Rambam Medical Center, B. Rappaport Faculty of Medicine, Technion Israel Institute of Technology Haifa, Israel.

出版信息

Harefuah. 2006 May;145(5):358-61, 397.

Abstract

The integrity and functional activity of the endothelial monolayer play a crucial role in the prevention of atherosclerosis. Extended endothelial cell damage by cardiovascular risk factors can result in endothelial cell apoptosis with loss of the integrity of the endothelium. Endothelial progenitor cells (EPCs) originating from the bone marrow play a significant role in neovascularization of ischemic tissues and in re-endothelialization of injured blood vessels. This may potentially limit atherosclerotic lesion formation. However, risk factors for coronary artery disease such as age and smoking, hypertension, hyperlipidemia and diabetes reduce the number and functional activity of these circulating endothelial progenitor cells, potentially restricting the therapeutic prospective of progenitor cells and limiting the regenerative capacity. The impairment of EPCs by risk factors may contribute to atherogenesis and atherosclerotic disease progression. The article reviews the role of EPCs as markers for atherosclerosis and cardiovascular outcomes and highlights possible novel strategies to interfere with the balance of injury and repair mechanisms.

摘要

内皮单层的完整性和功能活性在预防动脉粥样硬化中起着关键作用。心血管危险因素导致的内皮细胞损伤扩展可导致内皮细胞凋亡,进而丧失内皮的完整性。源自骨髓的内皮祖细胞(EPC)在缺血组织的新生血管形成以及受损血管的再内皮化过程中发挥着重要作用。这可能会潜在地限制动脉粥样硬化病变的形成。然而,诸如年龄、吸烟、高血压、高脂血症和糖尿病等冠状动脉疾病危险因素会减少这些循环内皮祖细胞的数量和功能活性,从而可能限制祖细胞的治疗前景并削弱再生能力。危险因素对EPC的损害可能会促进动脉粥样硬化的发生和动脉粥样硬化疾病的进展。本文综述了EPC作为动脉粥样硬化和心血管疾病预后标志物的作用,并强调了可能干扰损伤与修复机制平衡的新策略。

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