摘要
背景:如果仅仅基于传统的CV风险因素,心血管(CV)风险分层是次优的,因为具有相似风险特征的个体可能表现出不同的CV结果。因此,有必要确定新的风险因素。最近的研究强调内皮稳态在控制CV风险方面的相关性,但这些发现的临床相关性已经开始受到重视。深入了解参与这一现象的实际参与者将有助于识别新的生物标记物。内皮祖细胞(EPC)由于其在血管修复中的核心作用,有着广阔的应用前景。目的:由于过度炎症或免疫反应不平衡是EPC数量或功能改变的基础,可以推测这些介质可能被认为是危险分层的生物标志物。在本叙述性回顾中,我们的目的是汇编和批判性地评价目前所有将炎症和免疫途径与受损的EPC功能联系在一起的证据。结果:越来越多的证据表明,炎症驱动的传统CV危险因素与EPC功能障碍有关。衰老对EPC的影响与CXCR 4通路有关,而高血压则与肿瘤坏死因子α有关。观察到Akt/eNOS在糖尿病和血脂异常相关性状中的激活。炎症和氧化应激是EPC在吸烟过程中功能障碍的基础。结论:炎症和免疫网络可作为个性化药物方案中风险分层的可行生物标志物。
关键词: 内皮祖细胞,免疫系统,炎症,危险因素,血管修复,肿瘤坏死因子α。
Current Medicinal Chemistry
Title:EPC Dysfunction and Immune Networks: Translating Opportunities for Clinical Setting in Personalized Medicine
Volume: 25 Issue: 35
关键词: 内皮祖细胞,免疫系统,炎症,危险因素,血管修复,肿瘤坏死因子α。
摘要: Background: Cardiovascular (CV) risk stratification is suboptimal if solely based on traditional CV risk factors, since individuals with similar risk profiles could exhibit diverging CV outcomes. Thus, there is a need for new risk factors to be identified. Recent studies emphasize the relevance of the endothelial homeostasis in the control of CV risk, but the clinical relevance of these findings is starting to be appreciated. Gaining insight into the actual players involved in this phenomenon would lead to the identification of novel biomarkers. Due to their central role in vascular repair, Endothelial Progenitor Cells (EPC) are promising candidates for this issue.
Objective: Since excessive inflammation or imbalanced immune responses are known to underlie numerical or functional alterations of EPC, it can be speculated that these mediators may be considered as biomarkers for risk stratification. In the present narrative review, we aimed to compile and critically appraise all the current evidence linking inflammation and immune pathways with a compromised EPC functionality.
Results: A mounting body of evidence points to an inflammation-driven traditional CV risk factorsrelated EPC dysfunction. The effect of aging on EPC was associated with the CXCR4 pathway, whereas that of hypertension was related to TNFα. Activation of Akt/eNOS was observed in response to diabetes- and dyslipidemia-related traits. Inflammation and oxidative stress underlie the EPC dysfunction during smoking.
Conclusion: Inflammatory and immune networks can be proposed as feasible biomarkers for risk stratification in personalized medicine schemes.
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Cite this article as:
EPC Dysfunction and Immune Networks: Translating Opportunities for Clinical Setting in Personalized Medicine, Current Medicinal Chemistry 2018; 25 (35) . https://dx.doi.org/10.2174/0929867324666170606101823
DOI https://dx.doi.org/10.2174/0929867324666170606101823 |
Print ISSN 0929-8673 |
Publisher Name Bentham Science Publisher |
Online ISSN 1875-533X |
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