Novoyatleva Tatyana, Sajjad Amna, Engel Felix B
Department of Cardiac Development and Remodelling, Max-Planck-Institute for Heart and Lung Research , Bad Nauheim , Germany.
Department of Cardiac Development and Remodelling, Max-Planck-Institute for Heart and Lung Research , Bad Nauheim , Germany ; Government College University Faisalabad , Faisalabad , Pakistan.
Front Immunol. 2014 Feb 11;5:50. doi: 10.3389/fimmu.2014.00050. eCollection 2014.
Tumor necrosis factor (TNF) has been firmly established as a pathogenic factor in heart failure, a significant socio-economic burden. In this review, we will explore the role of other members of the TNF/TNF receptor superfamily (TNFSF/TNFRSF) in cardiovascular diseases (CVDs) focusing on TWEAK and its receptor Fn14, new players in myocardial remodeling and heart failure. The TWEAK/Fn14 pathway controls a variety of cellular activities such as proliferation, differentiation, and apoptosis and has diverse biological functions in pathological mechanisms like inflammation and fibrosis that are associated with CVDs. Furthermore, it has recently been shown that the TWEAK/Fn14 axis is a positive regulator of cardiac hypertrophy and that deletion of Fn14 receptor protects from right heart fibrosis and dysfunction. We discuss the potential use of the TWEAK/Fn14 axis as biomarker for CVDs as well as therapeutic target for future treatment of human heart failure based on supporting data from animal models and in vitro studies. Collectively, existing data strongly suggest the TWEAK/Fn14 axis as a potential new therapeutic target for achieving cardiac protection in patients with CVDs.
肿瘤坏死因子（TNF）已被确认为心力衰竭的致病因素，心力衰竭是一项重大的社会经济负担。在本综述中，我们将探讨TNF/TNF受体超家族（TNFSF/TNFRSF）的其他成员在心血管疾病（CVD）中的作用，重点关注肿瘤坏死因子样弱凋亡诱导因子（TWEAK）及其受体Fn14，它们是心肌重塑和心力衰竭中的新成员。TWEAK/Fn14信号通路控制着多种细胞活动，如增殖、分化和凋亡，并且在与CVD相关的炎症和纤维化等病理机制中具有多种生物学功能。此外，最近研究表明，TWEAK/Fn14轴是心脏肥大的正调节因子，并且Fn14受体的缺失可预防右心纤维化和功能障碍。基于动物模型和体外研究的支持数据，我们讨论了TWEAK/Fn14轴作为CVD生物标志物的潜在用途以及作为未来人类心力衰竭治疗靶点的可能性。总体而言，现有数据强烈表明TWEAK/Fn14轴是在CVD患者中实现心脏保护的潜在新治疗靶点。
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