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首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >Molecular evidence for arterial repair in atherosclerosis.
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Molecular evidence for arterial repair in atherosclerosis.

机译：动脉粥样硬化中动脉修复的分子证据。

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摘要

Atherosclerosis is a chronic inflammatory process and progresses through characteristic morphologic stages. We have shown previously that chronically injecting bone-marrow-derived vascular progenitor cells can effect arterial repair. This repair capacity depends on the age of the injected marrow cells, suggesting a progressive decline in progenitor cell function. We hypothesized that the progression of atherosclerosis coincides with the deteriorating repair capacity of the bone marrow. Here, we ascribe patterns of gene expression that accurately and reproducibly identify specific disease states in murine atherosclerosis. We then use these expression patterns to determine the point in the disease process at which the repair of arteries by competent bone marrow cells ceases to be efficient. We show that the loss of the molecular signature for competent repair is concurrent with the initiation of atherosclerotic lesions. This work provides a previously unreported comprehensive molecular data set using broad-based analysis that links the loss of successful repair with the progression of a chronic illness.
机译：动脉粥样硬化是一种慢性炎症过程，并通过特征性的形态学阶段发展。以前我们已经表明，长期注射骨髓来源的血管祖细胞可以影响动脉修复。这种修复能力取决于所注射的骨髓细胞的年龄，表明祖细胞功能逐渐下降。我们假设动脉粥样硬化的进展与骨髓修复能力的下降相吻合。在这里，我们归因于基因表达的模式，可以准确，可重复地识别鼠类动脉粥样硬化的特定疾病状态。然后，我们使用这些表达模式来确定疾病过程中主管骨髓细胞对动脉的修复不再有效的时间点。我们表明，丧失足够能力进行修复的分子特征是与动脉粥样硬化病变的开始同时发生的。这项工作使用广泛的分析提供了以前未报道的全面分子数据集，该分析将成功修复的损失与慢性病的发展联系起来。

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