Staudt Alexander, Landsberger Martin, Staudt Yvonne, Felix Stephan B
Klinik für Innere Medizin B, Ernst-Moritz-Arndt-Universität Greifswald, Germany.
Herz. 2002 Nov;27(7):691-8. doi: 10.1007/s00059-002-2420-5.
Cytokines are important mediators of the immune system and are of pathophysiological relevance for different cardiac diseases. Currently, 18 cytokines carrying the name interleukin (IL) are known; they can be subdivided into pro- and anti-inflammatory interleukins.
They partly act in a negative inotropic manner and cause destruction of cardiomyocytes resulting in myocardial fibrosis. The proinflammatory cytokine tumor necrosis factor (TNF-)alpha induces cardiodepressive effects and causes apoptosis. TNF-alpha, IL-6, soluble TNF-receptor-1 and -2 are independent predictors of increased mortality of patients with heart failure. Experimental and clinical evidence has shown that plasma and tissue levels of TNF-alpha were elevated to such extent as to explain at least some of the symptoms of heart failure due to the actions of this cytokine.
Two multicenter studies (RENAISSANCE, RECOVER), based on promising pilot studies, have disclosed no effect for the TNF-alpha antagonists (Etanercept) on mortality and morbidity. It is not possible, however, to draw the conclusion from the data of these studies that TNF-alpha plays no significant pathophysiological role in the etiology and progression of heart failure.
细胞因子是免疫系统的重要介质，在不同心脏疾病的病理生理学中具有相关性。目前，已知有18种细胞因子被命名为白细胞介素（IL）；它们可分为促炎和抗炎白细胞介素。
它们部分以负性变力方式起作用，导致心肌细胞破坏，进而引起心肌纤维化。促炎细胞因子肿瘤坏死因子（TNF）-α诱导心脏抑制作用并导致细胞凋亡。TNF-α、IL-6、可溶性TNF受体-1和-2是心力衰竭患者死亡率增加的独立预测因子。实验和临床证据表明，TNF-α的血浆和组织水平升高到足以解释至少部分由该细胞因子作用导致的心力衰竭症状的程度。
两项基于有前景的初步研究的多中心研究（复兴研究、康复研究）表明TNF-α拮抗剂（依那西普）对死亡率和发病率无影响。然而，不可能从这些研究的数据得出TNF-α在心力衰竭的病因和进展中不发挥重要病理生理作用的结论。
