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The Scientific World Journal
Volume 2013 (2013), Article ID 875363, 10 pages
Review Article

The Role of TNF-α and TNF Superfamily Members in the Pathogenesis of Calcific Aortic Valvular Disease

1Division of Cardiac Surgery, Department of Emergencies and Organ Transplantation (DETO), University of Bari “Aldo Moro”, Italy
2Department of Basic Medical Sciences, Neurosciences and Sense Organs, Section of Human Anatomy and Histology, University of Bari “Aldo Moro”, Piazza Giulio Cesare 11, 70124 Bari, Italy

Received 29 August 2013; Accepted 2 October 2013

Academic Editors: K. Awano, K. W. Lobdell, and I. Misumi

Copyright © 2013 Antonella Galeone et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Calcific aortic valve disease (CAVD) represents a slowly progressive pathologic process associated with major morbidity and mortality. The process is characterized by multiple steps: inflammation, fibrosis, and calcification. Numerous studies focalized on its physiopathology highlighting different “actors” for the multiple “acts.” This paper focuses on the role of the tumor necrosis factor superfamily (TNFSF) members in the pathogenesis of CAVD. In particular, we discuss the clinical and experimental studies providing evidence of the involvement of tumor necrosis factor-alpha (TNF-α), receptor activator of nuclear factor-kappa B (NF-κB) ligand (RANKL), its membrane receptor RANK and its decoy receptor osteoprotegerin (OPG), and TNF-related apoptosis-inducing ligand (TRAIL) in valvular calcification.