【摘 要】
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Endothelial progenitor cells (EPCs) were reported to repair the injured endothelium.However,they are vulnerable to the inflammatory environment represented by most vascular diseases including atheroth
【机 构】
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Zhejiang Chinese Medical University
【出 处】
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2016年浙江省医学会心电生理与起搏学术年会
论文部分内容阅读
Endothelial progenitor cells (EPCs) were reported to repair the injured endothelium.However,they are vulnerable to the inflammatory environment represented by most vascular diseases including atherothrombosis and pulmonary arterial hypertension.Elevated plasma concentrations of pro-inflammatory mediator soluble CD40 ligand (sCD40L) were one of the features of those inflammation-related diseases.Activation of CD40 pathway can reduce the numbers and impair the activities of EPCs,but the key mechanisms are still elusive.What is more,CD40 pathway was found to play a significant role in regulating nitric oxide (NO) bioavailability which was gaining widespread attention for its role in modulating various physiological processes of EPCs.We review recent work on how CD40 pathway influences EPC functions and NO bioavailability,discusstheir internal relations,and hypothesize that NO may be the key factor linking CD40 pathway to EPC dysfunction.Our hypothesis brings a new insight into the therapeutic function of NO in inflammatory conditions.Moreover,it may suggest us a new concept for the further clinical development of EPC transplantingtherapy.
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