寻找败血症诱导的心肌病的新生物标志物——需要克服的新挑战

C. Prepeliuc, Ionela-Larisa Miftode, Maria-Antoanela Pasare, R. Miftode, Lidia-Oana Stamateanu, I. Costache, A. Costache, E. Miftode
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引用次数: 0

摘要

脓毒症是一种由宿主对感染反应失调引起的危及生命的器官功能障碍,尽管最近取得了医学进展,但它仍然是全球危重患者最常见的死亡原因。败血症的心脏受累,更为人所知的是败血症诱导的心肌病,代表了败血症患者中发现的一种心脏功能障碍,其特征是心室扩张、心肌受累、射血分数降低和可逆性。尽管败血症中心脏受累的影响可能非常严重,但这种痛苦在文献中并没有引起激烈的争论。因此,为了更好地理解这种痛苦,我们需要识别新的标记。两种生物标志物,内皮素-1(ET-1)和可溶性抑瘤性2蛋白(sST2)先前已与败血症和急性/慢性心力衰竭有关。内皮素-1是氨基酸肽家族的一部分,主要由内皮细胞产生并发挥血管收缩作用,但也会导致血管细胞纤维化,刺激活性氧的产生并诱导促炎机制。在败血症期间,它诱导冠状动脉收缩,心输出量下降,血管阻力和通透性增加,在心脏水平上增加流入血管外空间的液体流量,并影响心肌细胞的收缩性。在大鼠感染性休克和内毒素诱导的发热反应中也发现了血清ET-1的高值。致瘤性抑制2蛋白(ST2)是白细胞介素-1受体家族的成员,参与T辅助细胞2的相关免疫反应。最近的研究发现ST2与炎症性疾病和心脏病之间存在密切联系。此外,它最近被美国食品药品监督管理局批准为心力衰竭的预后生物标志物,并被推荐用于评估额外的心血管风险。
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The search for novel biomarkers in sepsis-induced cardiomyopathy – A new challenge to overcome
Sepsis is a life-threatening organ dysfunction caused by a dysregulated host response to infection and it remains the most frequent cause of death amongst critically ill patients worldwide, despite recent medical advancements. The cardiac involvement in sepsis, better known as sepsis-induced cardiomyopathy, represents a form of cardiac dysfunction identified in septic patients, characterized by ventricular dilation, myocardial involvement, decreased ejection fraction and reversibility. Although the implications of cardiac involvement in sepsis can be extremely severe, this affliction has not been intensely debated in literature. Therefore, in order to better understand this affliction, we need to identify new markers. Two biomarkers, endothelin-1 (ET-1) and the soluble form of suppression of tumorigenicity 2 protein (sST2) have previously been linked to both sepsis and acute/chronic heart failure. Endothelin-1 is part of a family of amino acid peptides, that is mainly produced by endothelial cells and exerts a vasoconstrictive effect, but also causes fibrosis of the vascular cells, stimulates production of reactive oxygen species and induces proinflammatory mechanisms. During sepsis, it induces coronary vasoconstriction, decreased cardiac output, increased vascular resistance and permeability and increased fluid flux into the extravascular space on cardiac level, as well as affecting the contractility of myocardial myocytes. High values of serum ET-1 have also been identified in septic shock and in endotoxin-induced febrile responses in rats. The Suppression of tumorigenicity 2 protein (ST2) is a member of the interleukin-1 receptor family and is involved in T helper 2 cells-associated immune response. Recent studies identified a close link between ST2 and both inflammatory and heart diseases. Furthermore, it was recently approved by the Food and Drug Administration as a prognostic biomarker in heart failure and is recommended for the evaluation of additional cardiovascular risk.
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