Basic Mechanisms of Calcific Aortic Valve Disease

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 c...

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Published inCanadian journal of cardiology Vol. 30; no. 9; pp. 982 - 993
Main Authors Mathieu, Patrick, Boulanger, Marie-Chloé
Format Journal Article
LanguageEnglish
Published England Elsevier Inc 01.09.2014
Subjects
Online AccessGet full text
ISSN0828-282X
1916-7075
1916-7075
DOI10.1016/j.cjca.2014.03.029

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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. La calcification de la valve aortique (CVA) est le trouble des valves cardiaques le plus fréquent. Aucun traitement médical ne peut prévenir ou favoriser la régression de la CVA. Par conséquent, il est particulièrement important de définir et de comprendre les principaux mécanismes de base sous-jacents qui sont impliqués dans la CVA. Au cours de la dernière décennie, notre compréhension des fondements des processus menant à la CVA a progressé très rapidement. Par conséquent, notre compréhension des processus biopathologiques fondamentaux impliqués dans la CVA mènerait éventuellement à l’élaboration de nouveaux traitements pharmacologiques de la CAV. Dans cette revue, nous discutons des processus moléculaires qui sont impliqués dans la fibrose et la minéralisation de la valve aortique. Particulièrement, nous traitons du rôle de la rétention lipidique, de l’inflammation, de la signalisation du phosphate et de la transition ostéogène dans le développement de la CVA. Nous discutons des interactions entre ces différents processus et les voies de régulation principales ainsi que leur pertinence clinique.
AbstractList 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.
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. La calcification de la valve aortique (CVA) est le trouble des valves cardiaques le plus fréquent. Aucun traitement médical ne peut prévenir ou favoriser la régression de la CVA. Par conséquent, il est particulièrement important de définir et de comprendre les principaux mécanismes de base sous-jacents qui sont impliqués dans la CVA. Au cours de la dernière décennie, notre compréhension des fondements des processus menant à la CVA a progressé très rapidement. Par conséquent, notre compréhension des processus biopathologiques fondamentaux impliqués dans la CVA mènerait éventuellement à l’élaboration de nouveaux traitements pharmacologiques de la CAV. Dans cette revue, nous discutons des processus moléculaires qui sont impliqués dans la fibrose et la minéralisation de la valve aortique. Particulièrement, nous traitons du rôle de la rétention lipidique, de l’inflammation, de la signalisation du phosphate et de la transition ostéogène dans le développement de la CVA. Nous discutons des interactions entre ces différents processus et les voies de régulation principales ainsi que leur pertinence clinique.
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.
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.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.
Author Boulanger, Marie-Chloé
Mathieu, Patrick
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  fullname: Boulanger, Marie-Chloé
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Snippet 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....
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...
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SubjectTerms Aging - physiology
Aortic Valve - metabolism
Aortic Valve - pathology
Aortic Valve - physiopathology
Aortic Valve Stenosis - metabolism
Aortic Valve Stenosis - pathology
Aortic Valve Stenosis - physiopathology
Bone Morphogenetic Protein 2 - physiology
Calcinosis - metabolism
Calcinosis - pathology
Calcinosis - physiopathology
Cardiovascular
Endothelium - physiology
Humans
Inflammation - physiopathology
Interleukin-6 - physiology
Lipid Metabolism
Lipoproteins, HDL - physiology
Lipoproteins, LDL - metabolism
Nucleosides - metabolism
Nucleotides - metabolism
Phosphates - physiology
Phospholipases A2 - physiology
Receptors, Serotonin - physiology
Renin-Angiotensin System - physiology
RNA, Untranslated - physiology
Signal Transduction - physiology
Sirtuins - physiology
Stress, Mechanical
Transforming Growth Factor beta1 - physiology
Tumor Necrosis Factor-alpha - physiology
Title Basic Mechanisms of Calcific Aortic Valve Disease
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Volume 30
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