Contribution of Oxidative Stress (OS) in Calcific Aortic Valve Disease (CAVD): From Pathophysiology to Therapeutic Targets
Calcific aortic valve disease (CAVD) is a major cause of cardiovascular mortality and morbidity, with increased prevalence and incidence. The underlying mechanisms behind CAVD are complex, and are mainly illustrated by inflammation, mechanical stress (which induces prolonged aortic valve endothelial...
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MDPI AG
2022-08-01
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| Online Access: | https://www.mdpi.com/2073-4409/11/17/2663 |
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| author | Daniela Maria Tanase Emilia Valasciuc Evelina Maria Gosav Mariana Floria Claudia Florida Costea Nicoleta Dima Ionut Tudorancea Minela Aida Maranduca Ionela Lacramioara Serban |
| author_facet | Daniela Maria Tanase Emilia Valasciuc Evelina Maria Gosav Mariana Floria Claudia Florida Costea Nicoleta Dima Ionut Tudorancea Minela Aida Maranduca Ionela Lacramioara Serban |
| author_sort | Daniela Maria Tanase |
| collection | DOAJ |
| description | Calcific aortic valve disease (CAVD) is a major cause of cardiovascular mortality and morbidity, with increased prevalence and incidence. The underlying mechanisms behind CAVD are complex, and are mainly illustrated by inflammation, mechanical stress (which induces prolonged aortic valve endothelial dysfunction), increased oxidative stress (OS) (which trigger fibrosis), and calcification of valve leaflets. To date, besides aortic valve replacement, there are no specific pharmacological treatments for CAVD. In this review, we describe the mechanisms behind aortic valvular disease, the involvement of OS as a fundamental element in disease progression with predilection in AS, and its two most frequent etiologies (calcific aortic valve disease and bicuspid aortic valve); moreover, we highlight the potential of OS as a future therapeutic target. |
| first_indexed | 2024-03-10T01:56:46Z |
| format | Article |
| id | doaj.art-4cceb6b436a14d4eafa5f703b47e0590 |
| institution | Directory Open Access Journal |
| issn | 2073-4409 |
| language | English |
| last_indexed | 2024-03-10T01:56:46Z |
| publishDate | 2022-08-01 |
| publisher | MDPI AG |
| record_format | Article |
| series | Cells |
| spelling | doaj.art-4cceb6b436a14d4eafa5f703b47e05902023-11-23T12:54:50ZengMDPI AGCells2073-44092022-08-011117266310.3390/cells11172663Contribution of Oxidative Stress (OS) in Calcific Aortic Valve Disease (CAVD): From Pathophysiology to Therapeutic TargetsDaniela Maria Tanase0Emilia Valasciuc1Evelina Maria Gosav2Mariana Floria3Claudia Florida Costea4Nicoleta Dima5Ionut Tudorancea6Minela Aida Maranduca7Ionela Lacramioara Serban8Department of Internal Medicine, Grigore T. Popa University of Medicine and Pharmacy, 700115 Iasi, RomaniaDepartment of Internal Medicine, Grigore T. Popa University of Medicine and Pharmacy, 700115 Iasi, RomaniaDepartment of Internal Medicine, Grigore T. Popa University of Medicine and Pharmacy, 700115 Iasi, RomaniaDepartment of Internal Medicine, Grigore T. Popa University of Medicine and Pharmacy, 700115 Iasi, RomaniaDepartment of Ophthalmology, Faculty of Medicine, Grigore T. Popa University of Medicine and Pharmacy, 700115 Iasi, RomaniaDepartment of Internal Medicine, Grigore T. Popa University of Medicine and Pharmacy, 700115 Iasi, RomaniaDepartment of Morpho-Functional Sciences II, Discipline of Physiology, Grigore T. Popa University of Medicine and Pharmacy, 700115 Iasi, RomaniaInternal Medicine Clinic, St. Spiridon County Clinical Emergency Hospital Iasi, 700111 Iasi, RomaniaDepartment of Morpho-Functional Sciences II, Discipline of Physiology, Grigore T. Popa University of Medicine and Pharmacy, 700115 Iasi, RomaniaCalcific aortic valve disease (CAVD) is a major cause of cardiovascular mortality and morbidity, with increased prevalence and incidence. The underlying mechanisms behind CAVD are complex, and are mainly illustrated by inflammation, mechanical stress (which induces prolonged aortic valve endothelial dysfunction), increased oxidative stress (OS) (which trigger fibrosis), and calcification of valve leaflets. To date, besides aortic valve replacement, there are no specific pharmacological treatments for CAVD. In this review, we describe the mechanisms behind aortic valvular disease, the involvement of OS as a fundamental element in disease progression with predilection in AS, and its two most frequent etiologies (calcific aortic valve disease and bicuspid aortic valve); moreover, we highlight the potential of OS as a future therapeutic target.https://www.mdpi.com/2073-4409/11/17/2663oxidative stresscalcific aortic valve diseasebicuspid aortic valvevalvular interstitial cellsantioxidantstherapeutic targets |
| spellingShingle | Daniela Maria Tanase Emilia Valasciuc Evelina Maria Gosav Mariana Floria Claudia Florida Costea Nicoleta Dima Ionut Tudorancea Minela Aida Maranduca Ionela Lacramioara Serban Contribution of Oxidative Stress (OS) in Calcific Aortic Valve Disease (CAVD): From Pathophysiology to Therapeutic Targets Cells oxidative stress calcific aortic valve disease bicuspid aortic valve valvular interstitial cells antioxidants therapeutic targets |
| title | Contribution of Oxidative Stress (OS) in Calcific Aortic Valve Disease (CAVD): From Pathophysiology to Therapeutic Targets |
| title_full | Contribution of Oxidative Stress (OS) in Calcific Aortic Valve Disease (CAVD): From Pathophysiology to Therapeutic Targets |
| title_fullStr | Contribution of Oxidative Stress (OS) in Calcific Aortic Valve Disease (CAVD): From Pathophysiology to Therapeutic Targets |
| title_full_unstemmed | Contribution of Oxidative Stress (OS) in Calcific Aortic Valve Disease (CAVD): From Pathophysiology to Therapeutic Targets |
| title_short | Contribution of Oxidative Stress (OS) in Calcific Aortic Valve Disease (CAVD): From Pathophysiology to Therapeutic Targets |
| title_sort | contribution of oxidative stress os in calcific aortic valve disease cavd from pathophysiology to therapeutic targets |
| topic | oxidative stress calcific aortic valve disease bicuspid aortic valve valvular interstitial cells antioxidants therapeutic targets |
| url | https://www.mdpi.com/2073-4409/11/17/2663 |
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