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首页> 外文期刊>Journal of Medical Biochemistry >Inflammatory and Apoptotic Markers in Ischemic Heart Disease Patients
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Inflammatory and Apoptotic Markers in Ischemic Heart Disease Patients

机译：缺血性心脏病患者的炎症和凋亡标志物

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Inflammatory and Apoptotic Markers in Ischemic Heart Disease PatientsIschemic heart disease is the most frequent cause of cardiovascular morbidity and mortality. It is developed on the basis of atherosclerosis which is today considered a chronic inflammatory disease. It is documented by an increase in inflammatory and immune biomarkers, such as C-reactive protein, fibrinogen, neopterin, leukocytes, lymphocytes and others, that are significantly changed in patients with unstable angina or acute myocardial infarction. CRP is mostly studied. Increased concentrations of CRP are associated with a series of risk factors. CRP may predict recurrent events and mortality independently of cardiac troponin levels, and it is also an independent predictor of a cardiovascular event after adjustment for traditional risk factors. Although CRP currently appears to be the most promising biological marker, there is still controversy regarding its use in clinical practice. Both necrotic and apoptotic cell death are documented during atherogenesis, however, limited data are available about apoptotic markers in ischemic heart disease patients. Increasing evidence supports the existence of apoptotic death initiated by ligation of membrane-bound death receptors or by release of cytochrome c from mitochondria, as well as their regulators in the heart. The studies of serum markers show that the apoptotic process is disregulated in ischemic heart disease patients. Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) is present in stable atherosclerotic lesions, is increased in vulnerable plaques, but its serum levels are reduced significantly in patients with unstable angina. Serum Fas concentrations are increased and FasL are decreased in subjects at high cardiovascular risk. The results of our study show significant changes in serum Fas, FasL, and Bcl-2 concentrations, and lymphocyte caspase-3 activity in different stages of ischemic heart disease. For now, there is evidence that statins are effective in the regulation of some apoptotic markers. The better understanding of the pathways of apoptosis and their regulation is promissing in yielding novel therapeutic targets for cardiovascular disease.
机译：缺血性心脏病患者的炎症和凋亡标志物缺血性心脏病是心血管疾病发病率和死亡率的最常见原因。它是在动脉粥样硬化的基础上发展起来的，如今已被认为是一种慢性炎症性疾病。炎症和免疫生物标志物（例如C反应蛋白，纤维蛋白原，新蝶呤，白细胞，淋巴细胞等）的增加已被证明，在不稳定型心绞痛或急性心肌梗死的患者中，这些标志物发生了明显变化。对CRP的研究最多。 CRP浓度升高与一系列风险因素有关。 CRP可以独立于心脏肌钙蛋白水平预测复发事件和死亡率，并且在调整了传统危险因素后，它还是心血管事件的独立预测因子。尽管CRP目前似乎是最有前途的生物标志物，但在临床实践中仍存在争议。动脉粥样硬化发生期间既有坏死性细胞死亡也有凋亡性细胞死亡，但是，关于缺血性心脏病患者凋亡标记物的数据有限。越来越多的证据支持通过连接膜结合死亡受体或从线粒体释放细胞色素c及其心脏调节剂引发的细胞凋亡。血清标志物的研究表明，缺血性心脏病患者的细胞凋亡过程受到了破坏。肿瘤坏死因子相关的凋亡诱导配体（TRAIL）存在于稳定的动脉粥样硬化病变中，在易损斑块中有所增加，但在不稳定型心绞痛患者中其血清水平显着降低。具有高心血管风险的受试者的血清Fas浓度升高而FasL降低。我们的研究结果显示在缺血性心脏病不同阶段，血清Fas，FasL和Bcl-2浓度以及淋巴细胞caspase-3活性发生了显着变化。目前，有证据表明他汀类药物可有效调节某些凋亡标记物。在产生新的心血管疾病治疗靶点方面，人们对细胞凋亡的途径及其调控的更好的理解是必然的。

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