Next Article in Journal
mTOR Regulation of Metabolism in Hematologic Malignancies
Next Article in Special Issue
Intravenous Administration of Allogenic Cell-Derived Microvesicles of Healthy Origins Defend Against Atherosclerotic Cardiovascular Disease Development by a Direct Action on Endothelial Progenitor Cells
Previous Article in Journal
Future Therapeutic Directions for Smac-Mimetics
Previous Article in Special Issue
Secreted Phospholipase A2-IIA Modulates Transdifferentiation of Cardiac Fibroblast through EGFR Transactivation: An Inflammation–Fibrosis Link
Open AccessReview

Tumor Necrosis Factor-Like Weak Inducer of Apoptosis (TWEAK)/Fibroblast Growth Factor-Inducible 14 (Fn14) Axis in Cardiovascular Diseases: Progress and Challenges

Vascular Research Lab, IIS-Fundación Jiménez Díaz University Hospital and CIBERCV, Av. Reyes Católicos 2, 28040 Madrid, Spain
*
Authors to whom correspondence should be addressed.
Cells 2020, 9(2), 405; https://doi.org/10.3390/cells9020405 (registering DOI)
Received: 21 January 2020 / Revised: 6 February 2020 / Accepted: 7 February 2020 / Published: 11 February 2020
(This article belongs to the Special Issue Cells in Cardiovascular Disease)
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.
Keywords: TWEAK; Fn14; vascular remodeling; stroke; heart failure TWEAK; Fn14; vascular remodeling; stroke; heart failure
MDPI and ACS Style

Méndez-Barbero, N.; Gutiérrez-Muñoz, C.; Blázquez-Serra, R.; Martín-Ventura, J.L.; Blanco-Colio, L.M. Tumor Necrosis Factor-Like Weak Inducer of Apoptosis (TWEAK)/Fibroblast Growth Factor-Inducible 14 (Fn14) Axis in Cardiovascular Diseases: Progress and Challenges. Cells 2020, 9, 405.

Show more citation formats Show less citations formats
Note that from the first issue of 2016, MDPI journals use article numbers instead of page numbers. See further details here.

Article Access Map by Country/Region

1
Back to TopTop