TWEAK-Fn14: a promising target for cardio-cerebrovascular diseases and brain-heart syndrome

Read full text
Authors: Qinglin Fei, Jun Chang, Tingcan Jiang, Guoqiang Guan, Yujuan Liang, Cuicui Cheng, Guangxu Xiao, Qiuyan Guo, Guanwei Fan, Yan Zhu, Ming Lyu
Cited by: 1
References: 215

Abstract

Cardio-cerebrovascular diseases (CCVDs), notably stroke and coronary heart disease, represent the leading causes of mortality and disability worldwide. The intricate bidirectional feedback between the brain and heart in brain-heart syndrome (BHS) exacerbates clinical outcomes and imposes a significant economic burden on patients. The cytokine tumor necrosis factor-like apoptosis weak inducer (TWEAK) and its receptor fibroblast growth factor-inducible 14 (Fn14) are overexpressed in cerebral injury and cardiac dysfunction. Elevated levels of TWEAK and Fn14 contribute to the development of various brain diseases, including blood-brain barrier damage, brain edema, neuroinflammation, neuronal apoptosis, and neurodegeneration. Additionally, the TWEAK-Fn14 axis is implicated in numerous pathophysiological events in the heart, such as cardiomyocyte proliferation, inflammation, apoptosis, hypertrophy, fibrosis, contractile function disruption, and ventricular dilatation. Given its significant contributions to CCVDs, the TWEAK-Fn14 axis has also emerged as a promising therapeutic target for BHS. In this review, the critical roles of TWEAK-Fn14 in CCVDs and its potential interplay between the brain-heart axis in BHS were updated and discussed, which shed a new light on co-treatment of brain and heart and brain-heart syndrome.

Fields of Study & Subjects

NF-κB Signaling Pathways FOXO transcription factor regulation TGF-β signaling in diseases

Publication details

Journal / source
Frontiers in Immunology
Publisher
Frontiers Media SA
Volume
16
Pages
1710055–1710055
Publication date
1 April 2026
Language
EN