title: Basic mechanisms of calcific aortic valve disease.
abstract: Calcific aortic valve disease (CAVD) is the most common heart valve disorder. There is no medical treatment to prevent and/or promote the regression of CAVD. Hence, it is of foremost importance to delineate and understand the key basic underlying mechanisms involved in CAVD. In the past decade our comprehension of the underpinning processes leading to CAVD has expanded at a fast pace. Hence, our understanding of the basic pathobiological processes implicated in CAVD might lead eventually to the development of novel pharmaceutical therapies for CAVD. In this review, we discuss molecular processes that are implicated in fibrosis and mineralization of the aortic valve. Specifically, we address the role of lipid retention, inflammation, phosphate signalling and osteogenic transition in the development of CAVD. Interplays between these different processes and the key regulation pathways are discussed along with their clinical relevance.
authors.affiliation: Laboratoire d'Études Moléculaires des Valvulopathies (LEMV), Groupe de Recherche en Valvulopathies (GRV), Québec Heart and Lung Institute/Research Center, Department of Surgery, Laval University, Québec, Québec, Canada. Electronic address: patrick.mathieu@chg.ulaval.ca.
authors.forename: Patrick
authors.initials: P
authors.lastname: Mathieu
authors.affiliation: Laboratoire d'Études Moléculaires des Valvulopathies (LEMV), Groupe de Recherche en Valvulopathies (GRV), Québec Heart and Lung Institute/Research Center, Department of Surgery, Laval University, Québec, Québec, Canada.
authors.forename: Marie-Chloé
authors.initials: MC
authors.lastname: Boulanger
mesh_terms: D000375:Aging / Q000502:physiology; D001021:Aortic Valve / Q000378:metabolism / Q000473:pathology* / Q000503:physiopathology; D001024:Aortic Valve Stenosis / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology*; D055396:Bone Morphogenetic Protein 2 / Q000502:physiology; D002114:Calcinosis / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology*; D004727:Endothelium / Q000502:physiology; D006801:Humans; D007249:Inflammation / Q000503:physiopathology; D015850:Interleukin-6 / Q000502:physiology; D050356:Lipid Metabolism; D008075:Lipoproteins, HDL / Q000502:physiology; D008077:Lipoproteins, LDL / Q000378:metabolism; D009705:Nucleosides / Q000378:metabolism; D009711:Nucleotides / Q000378:metabolism; D010710:Phosphates / Q000502:physiology; D054467:Phospholipases A2 / Q000502:physiology; D022661:RNA, Untranslated / Q000502:physiology; D011985:Receptors, Serotonin / Q000502:physiology; D012084:Renin-Angiotensin System / Q000502:physiology; D015398:Signal Transduction / Q000502:physiology; D037761:Sirtuins / Q000502:physiology; D013314:Stress, Mechanical; D053773:Transforming Growth Factor beta1 / Q000502:physiology; D014409:Tumor Necrosis Factor-alpha / Q000502:physiology
chemical_list: C525718:BMP2 protein, human; D055396:Bone Morphogenetic Protein 2; D015850:Interleukin-6; D008075:Lipoproteins, HDL; D008077:Lipoproteins, LDL; D009705:Nucleosides; D009711:Nucleotides; D010710:Phosphates; D022661:RNA, Untranslated; D011985:Receptors, Serotonin; D053773:Transforming Growth Factor beta1; D014409:Tumor Necrosis Factor-alpha; D054467:Phospholipases A2; D037761:Sirtuins