白细胞介素-6与心血管疾病。

Tsugiyasu Kanda, Takashi Takahashi
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引用次数: 249

摘要

炎症细胞因子对心血管科学家和临床医生都很重要。白细胞介素-6 (IL-6)在充血性心力衰竭(CHF)患者循环和心内IL-6水平升高的报道中得到了强调。IL-6可能参与多种原因引起的慢性心力衰竭综合征心肌损伤和功能障碍的进展。作为心肌病、心肌炎、同种异体移植排斥反应和左心室辅助装置(lvad)条件下CHF的原因,循环IL-6水平与左心室功能障碍的严重程度相关,也是随后临床结果的有力预测指标。在病毒性心肌炎下,IL-6的持续和过量产生通过破坏细胞因子网络和病毒清除来促进心肌损伤。尽管IL-6在病毒抗原呈递过程中可能很重要,但在病毒性心肌炎动物模型中,免疫应答的早期激活和病毒复制的衰减似乎也很重要。IL-6可通过IL-6信号转导受体成分糖蛋白130引起心肌肥厚。有几个有趣的病例心脏黏液瘤合并纵隔淋巴结病或左心室肥厚。供体心肌IL-6表达升高,均有明显的功能障碍。与晚期心力衰竭患者相比,LVAD患者的心肌IL-6浓度也显著升高。尽管IL-6家族在心血管疾病的病理生理中起着核心作用,但IL-6家族是有益还是有害仍有待确定。未来的研究将需要解决这个问题。
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Interleukin-6 and cardiovascular diseases.

Inflammatory cytokines are important for both cardiovascular scientists and practicing clinicians. Interleukin-6 (IL-6) has been emphasized by reports of elevated circulating as well as intracardiac IL-6 levels in patients with congestive heart failure (CHF). IL-6 may contribute to the progression of myocardial damage and dysfunction in chronic heart failure syndrome resulting from different causes. As the cause of CHF in cardiomyopathy, myocarditis, allograft rejection, and left ventricular assist device (LVADs) conditions, circulating IL-6 levels are associated with the severity of left ventricular dysfunction, and are also strong predictors of subsequent clinical outcomes. Continuous and excessive production of IL-6 promotes myocardial injury by breaking down both cytokine networks and viral clearance under viral myocarditis. Although IL-6 is likely important in the process of viral antigen presentation, early activation of immune responses and attenuation of viral replication also appear to be significant in an animal model of viral myocarditis. IL-6 can cause cardiac hypertrophy through the IL-6 signal transducing receptor component, glycoprotein 130. There are several interesting cases of cardiac myxoma complicated with mediastinal lymphadenopathy or left ventricular hypertrophy. Increased expression of IL-6 is observed in the myocardium of all donor hearts showing marked dysfunction. Myocardial IL-6 concentrations are also significantly higher in LVAD candidates compared with advanced heart failure patients. Although the IL-6 family plays a central role in the pathophysiology of cardiovascular diseases, it remains to be determined whether the IL-6 family is beneficial or detrimental. Future study will be needed to resolve this question.

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