Bone marrow stem cells regenerate infarcted myocardium

Bone marrow stem cells regenerate infarcted myocardium
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DOI:
10.1034/j.1399-3046.7.s3.13.x
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发表时间:
2003-01-01
影响因子:
1.3
通讯作者:
Anversa, P
Anversa, P
中科院分区:
医学4区
文献类型:
--
作者:
Orlic, D;Kajstura, J;Anversa, P

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心脏病是美国男性和女性的主要死因。近50%的心血管死亡是由冠状动脉疾病引起的。左冠状动脉闭塞会导致受影响的心肌组织的缺血、梗死和坏死,随后会形成疤痕和丧失功能。虽然存活心肌中的心肌细胞肥大,细胞分裂发生在死亡组织的边缘区域,但心肌梗死不会再生,最终导致个体死亡。在动物模型和人类中,已经进行了许多修复受损心肌的尝试。骨髓干细胞(BMSC)在成人一生中保持自我更新和分化为所有血统细胞的能力。这些成年的骨髓间充质干细胞最近被证明具有在骨髓以外的组织中分化为多种特定细胞类型的能力。我们的研究集中在成年小鼠诱导的心肌梗死后,骨髓间充质干细胞形成新的心肌细胞和冠状动脉的能力。在这篇文章中,我们将回顾我们之前发表的关于BMSC在急性缺血性心肌损伤中再生能力的研究数据。在一个实验中,供体骨髓间充质干细胞被直接注射到左心室损伤区域附近的健康心肌中。在第二个实验中,根据干细胞将运输到心肌梗死的理论,对小鼠进行细胞因子治疗,以动员其BMSC进入循环。在两种实验方案中,骨髓间充质干细胞都长出了新的心肌细胞和冠状动脉血管。这种来自骨髓间充质干细胞的心肌再生导致了心功能和存活率的改善。
Heart disease is the leading cause of death in the United States for both men and women. Nearly 50% of all cardiovascular deaths result from coronary artery disease. Occlusion of the left coronary artery leads to ischemia, infarction, necrosis of the affected myocardial tissue followed by scar formation and loss of function. Although myocytes in the surviving myocardium undergo hypertrophy and cell division occurs in the border area of the dead tissue, myocardial infarcts do not regenerate and eventually result in the death of the individual. Numerous attempts have been made to repair damaged myocardium in animal models and in humans. Bone marrow stem cells (BMSC) retain the ability throughout adult life to self-renew and differentiate into cells of all blood lineages. These adult BMSC have recently been shown to have the capacity to differentiate into multiple specific cell types in tissues other than bone marrow. Our research is focused on the capacity of BMSC to form new cardiac myocytes and coronary vessels following an induced myocardial infarct in adult mice. In this paper we will review the data we have previously published from studies on the regenerative capacity of BMSC in acute ischemic myocardial injury. In one experiment donor BMSC were injected directly into the healthy myocardium adjacent to the injured area of the left ventricle. In the second experiment, mice were treated with cytokines to mobilize their BMSC into the circulation on the theory that the stem cells would traffic to the myocardial infarct. In both experimental protocols, the BMSC gave rise to new cardiac myocytes and coronary blood vessels. This BMSC-derived myocardial regeneration resulted in improved cardiac function and survival.