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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.

Competing Interests: The authors declare no conflict of interest.

Titel:	Tumor Necrosis Factor-Like Weak Inducer of Apoptosis (TWEAK)/Fibroblast Growth Factor-Inducible 14 (Fn14) Axis in Cardiovascular Diseases: Progress and Challenges.
Autor/in / Beteiligte Person:	Méndez-Barbero, N ; Gutiérrez-Muñoz, C ; Blázquez-Serra, R ; Martín-Ventura, JL ; Blanco-Colio, LM
Link:	Full Text Finder (Volltext)
Zeitschrift:	Cells, Jg. 9 (2020-02-11), Heft 2
Veröffentlichung:	Basel, Switzerland : MDPI, 2020
Medientyp:	academicJournal
ISSN:	2073-4409 (electronic)
DOI:	10.3390/cells9020405
Schlagwort:	Apoptosis genetics Cardiovascular Diseases pathology Heart Disease Risk Factors Humans Inflammation pathology Signal Transduction genetics Ventricular Remodeling genetics Cardiovascular Diseases genetics Cytokine TWEAK genetics Inflammation genetics TWEAK Receptor genetics
Sonstiges:	Nachgewiesen in: MEDLINE Sprachen: English Publication Type: Journal Article; Research Support, Non-U.S. Gov't; Review Language: English [Cells] 2020 Feb 11; Vol. 9 (2). <i>Date of Electronic Publication: </i>2020 Feb 11. MeSH Terms: Cardiovascular Diseases / genetics ; Cytokine TWEAK / genetics ; Inflammation / genetics ; TWEAK Receptor / genetics ; Apoptosis / genetics ; Cardiovascular Diseases / pathology ; Heart Disease Risk Factors ; Humans ; Inflammation / pathology ; Signal Transduction / genetics ; Ventricular Remodeling / genetics References: Arterioscler Thromb Vasc Biol. 2006 Dec;26(12):2605-13. (PMID: 16973970) ; J Cereb Blood Flow Metab. 2003 Aug;23(8):879-94. (PMID: 12902832) ; Mol Immunol. 2017 Jul;87:67-75. (PMID: 28411440) ; Cytokine Growth Factor Rev. 2003 Jun-Aug;14(3-4):241-9. (PMID: 12787562) ; J Thorac Cardiovasc Surg. 2011 Dec;142(6):1567-74. (PMID: 21996300) ; Arterioscler Thromb Vasc Biol. 2013 Apr;33(4):718-26. 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(PMID: 19887380) Contributed Indexing: Keywords: Fn14; TWEAK; heart failure; stroke; vascular remodeling Substance Nomenclature: 0 (Cytokine TWEAK) ; 0 (TNFRSF12A protein, human) ; 0 (TNFSF12 protein, human) ; 0 (TWEAK Receptor) Entry Date(s): Date Created: 20200215 Date Completed: 20210226 Latest Revision: 20210226 Update Code: 20240513 PubMed Central ID: PMC7072601

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