Abstract
Cardiovascular diseases (CVD) are the leading cause of mortality in Western countries. CVD include several pathologies, such as coronary artery disease, stroke, peripheral artery disease, and aortic aneurysm, among others. All of them are characterized by a pathological vascular remodeling in which inflammation plays a key role. Interaction between different members of the tumor necrosis factor superfamily and their cognate receptors induce several biological actions that may participate in CVD. The cytokine tumor necrosis factor-like weak inducer of apoptosis (TWEAK) and its functional receptor, fibroblast growth factor-inducible 14 (Fn14), are abundantly expressed during pathological cardiovascular remodeling. The TWEAK/Fn14 axis controls a variety of cellular functions, such as proliferation, differentiation, and apoptosis, and has several biological functions, such as inflammation and fibrosis that are linked to CVD. It has been demonstrated that persistent TWEAK/Fn14 activation is involved in both vessel and heart remodeling associated with acute and chronic CVD. In this review, we summarized the role of the TWEAK/Fn14 axis during pathological cardiovascular remodeling, highlighting the cellular components and the signaling pathways that are involved in these processes.
Highlights
Cardiovascular diseases (CVD) are the main cause of death in developed countries, despite the fact that cardiovascular diseases (CVDs) rates and case-fatality rates have fallen considerably over the last two decades in those countries
Tumor necrosis factor-like weak inducer of apoptosis (TWEAK) and its sole functional receptor fibroblast growth factor-inducible 14 (Fn14) are two members of the tumor necrosis factor (TNF) superfamily that participate in multiple biological activities, including proliferation, migration, differentiation, apoptosis, angiogenesis, and inflammation [6]
tumor necrosis factor-like weak inducer of apoptosis (TWEAK) and Fn14 are closely related in humans and mice, being that their homology is higher than 90%
Summary
Cardiovascular diseases (CVD) are the main cause of death in developed countries, despite the fact that CVD rates and case-fatality rates have fallen considerably over the last two decades in those countries. CVD accounts for 17.3 million deaths per year, a number that is expected to grow to more than 23.6 million by 2030 [1]. Tumor necrosis factor-like weak inducer of apoptosis (TWEAK) and its sole functional receptor fibroblast growth factor-inducible 14 (Fn14) are two members of the TNF superfamily that participate in multiple biological activities, including proliferation, migration, differentiation, apoptosis, angiogenesis, and inflammation [6]. All of these processes are closely related to pathological cardiovascular remodeling
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