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Restoring stem cell mobilization to promote vascular repair in diabetes

机译:恢复干细胞动员以促进糖尿病的血管修复

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摘要

Diabetes triggers endothelial dysfunction, which is linked to increased risk of cardiovascular diseases. Stem and progenitor cells from the bone marrow are involved in the maintenance of vascular integrity. Diabetic patients show a dysfunction of these cells, which might represent a novel pathophysiological mechanism of vascular disease. Specifically, stem and progenitor cells fail to egress from the bone marrow (BM) due to BM pathological alterations and unresponsiveness to mobilizing stimuli. In this review, we describe impaired stem cell mobilization in diabetes as a mechanism of failed vascular repair and we provide evidence that pharmacological strategies can restore mobilization. We discuss recent advances in the knowledge of aberrant organization of the diabetic BM and its implications for impaired mobilization. Finally, we describe in detail the pharmacological exploitation of the G-CSF/DPP-4(CD26)/SDF-1α axis as a novel strategy to improve mobilization and attain vascular repair in diabetes.
机译:糖尿病引发内皮功能障碍,这与心血管疾病的风险增加有关。骨髓的干细胞和祖细胞参与血管完整性的维持。糖尿病患者显示这些细胞功能异常,这可能代表了血管疾病的新型病理生理机制。具体而言,由于BM病理改变以及对动员刺激无反应,干细胞和祖细胞未能从骨髓(BM)流出。在这篇综述中,我们将糖尿病中干细胞的动员描述为血管修复失败的机制,并提供了药理学策略可以恢复动员的证据。我们讨论了糖尿病BM异常组织的知识及其对动员障碍的影响的最新进展。最后,我们详细描述了G-CSF / DPP-4(CD26)/SDF-1α轴的药理开发,以此作为改善糖尿病动员和获得血管修复的新策略。

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