Yndestad Arne, Damås Jan Kristian, Øie Erik, Ueland Thor, Gullestad Lars, Aukrust Pål
Section of Clinical Immunology and Infectious Diseases, Medical Department, Rikshospitalet-Radiumhospitalet Medical Center, Sognsvannsveien 20, N-0027 Oslo, Norway.
Curr Cardiol Rep. 2007 May;9(3):236-41. doi: 10.1007/BF02938356.
Chronic heart failure (HF) is a disorder characterized in part by immune activation and inflammation. Thus, patients with HF have elevated levels of a number of inflammatory cytokines, both in the circulation and in the failing heart itself. Several mechanisms for this immune activation, which are not mutually exclusive, have been suggested, including neurohormonal activation, hemodynamic overload, and activation of the innate immune system secondary to cardiac stress. Importantly, experimental studies have shown that inflammatory cytokines such as tumor necrosis factor-alpha, interleukin-1b, and monocyte chemoattractant peptide-1 may contribute to the development and progression of HF by promoting myocardial hypertrophy, activating matrix metalloproteinases, provoking contractile dysfunction, and inducing apoptosis. However, inflammatory cytokines may also have adaptive and cardioprotective effects. This important aspect of cytokine biology must be kept in mind when designing new immunomodulatory treatment modalities in HF.
慢性心力衰竭（HF）是一种部分以免疫激活和炎症为特征的病症。因此，HF患者体内多种炎症细胞因子的水平在循环系统以及衰竭心脏本身中均有所升高。对于这种免疫激活，已提出多种并非相互排斥的机制，包括神经激素激活、血流动力学过载以及心脏应激继发的先天性免疫系统激活。重要的是，实验研究表明，诸如肿瘤坏死因子-α、白细胞介素-1β和单核细胞趋化蛋白-1等炎症细胞因子可能通过促进心肌肥大、激活基质金属蛋白酶、引发收缩功能障碍以及诱导细胞凋亡，从而促进HF的发生和发展。然而，炎症细胞因子也可能具有适应性和心脏保护作用。在设计针对HF的新型免疫调节治疗方案时，必须牢记细胞因子生物学的这一重要方面。
