Role for Galectin-3 in Calcific Aortic Valve Stenosis.

Date publication

novembre 2016

Journal

Journal of the American Heart Association

Auteurs

Membres identifiés du Cancéropôle Est :
Pr ROSSIGNOL Patrick

Tous les auteurs :
Sádaba JR, Martínez-Martínez E, Arrieta V, Álvarez V, Fernández-Celis A, Ibarrola J, Melero A, Rossignol P, Cachofeiro V, López-Andrés N

Lien Pubmed

https://www.ncbi.nlm.nih.gov/pubmed/27815266

Résumé

Aortic stenosis (AS) is a chronic inflammatory disease, and calcification plays an important role in the progression of the disease. Galectin-3 (Gal-3) is a proinflammatory molecule involved in vascular osteogenesis in atherosclerosis. Therefore, we hypothesized that Gal-3 could mediate valve calcification in AS.

Mots clés

Aged, Aged, 80 and over, Antigens, CD, metabolism, Antigens, Differentiation, Myelomonocytic, metabolism, Aortic Valve, metabolism, Aortic Valve Stenosis, metabolism, B7-1 Antigen, metabolism, Blotting, Western, Bone Morphogenetic Protein 2, metabolism, CRISPR-Cas Systems, Calcinosis, metabolism, Case-Control Studies, Cell Differentiation, Core Binding Factor Alpha 1 Subunit, metabolism, Female, Galectin 3, genetics, Gene Knockdown Techniques, Heart Valve Prosthesis Implantation, Humans, In Vitro Techniques, Male, Osteoblasts, Osteopontin, metabolism, Pectins, pharmacology, Prospective Studies, Real-Time Polymerase Chain Reaction, Reverse Transcriptase Polymerase Chain Reaction, SOX9 Transcription Factor, metabolism, Tumor Necrosis Factor-alpha, metabolism

Référence

J Am Heart Assoc. 2016 Nov 4;5(11):