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 in | Canadian journal of cardiology Vol. 30; no. 9; pp. 982 - 993 |
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Main Authors | , |
Format | Journal Article |
Language | English |
Published |
England
Elsevier Inc
01.09.2014
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Subjects | |
Online Access | Get full text |
ISSN | 0828-282X 1916-7075 1916-7075 |
DOI | 10.1016/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. |
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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 |
Author_xml | – sequence: 1 givenname: Patrick surname: Mathieu fullname: Mathieu, Patrick email: patrick.mathieu@chg.ulaval.ca – sequence: 2 givenname: Marie-Chloé surname: Boulanger fullname: Boulanger, Marie-Chloé |
BackLink | https://www.ncbi.nlm.nih.gov/pubmed/25085215$$D View this record in MEDLINE/PubMed |
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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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