ArticleOxidative medicine and cellular longevity2020
Semicarbazide-Sensitive Amine Oxidase Increases in Calcific Aortic Valve Stenosis and Contributes to Valvular Interstitial Cell Calcification.
Article in Oxidative medicine and cellular longevity, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 26 citations in OpenAlex.
- The role of VAP-1 in cardiovascular disease: a review.Frontiers in cardiovascular medicine · 2025Review
- Helicobacter Pylori Virulence Factor Cytotoxin-Associated Gene A (CagA) Induces Vascular Calcification in Coronary Artery Smooth Muscle Cells.International journal of molecular sciences · 2023Article
- The Biological Implication of Semicarbazide-Sensitive Amine Oxidase (SSAO) Upregulation in Rat Systemic Inflammatory Response under Simulated Aerospace Environment.International journal of molecular sciences · 2023Article
- Development and validation of a new prediction model for calcific aortic valve stenosis.Journal of thoracic disease · 2022Article
- Review
- Role of oxidative stress in calcific aortic valve disease and its therapeutic implications.Cardiovascular research · 2022Review
- Calcific aortic valve stenosis and COVID-19: clinical management, valvular damage, and pathophysiological mechanisms.Cardiology plus · 2022Review
- Increased atherosclerotic plaque in AOC3 knock-out in ApoEFrontiers in cardiovascular medicine · 2022Article
- The mechanistic pathways of oxidative stress in aortic stenosis and clinical implications.Theranostics · 2022Review
- Iron in Cardiovascular Disease: Challenges and Potentials.Frontiers in cardiovascular medicine · 2021Review
- Telomere Length in Valve Tissue Is Shorter in Individuals With Aortic Stenosis and in Calcified Valve Areas.Frontiers in cell and developmental biology · 2021Article
- Vascular Adhesion Protein-1 (VAP-1)/Semicarbazide-Sensitive Amine Oxidase (SSAO): A Potential Therapeutic Target for Atherosclerotic Cardiovascular Diseases.Frontiers in pharmacology · 2021Review
- Omega-3 Polyunsaturated Fatty Acids Decrease Aortic Valve Disease Through the Resolvin E1 and ChemR23 Axis.Circulation · 2020Article
- TLR7 Expression Is Associated with M2 Macrophage Subset in Calcific Aortic Valve Stenosis.Cells · 2020Article
- Review
- Article
- Omega-3 Polyunsaturated Fatty Acids and the Resolution of Inflammation: Novel Therapeutic Opportunities for Aortic Valve Stenosis?Frontiers in cell and developmental biology · 2020Review
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Authors and funding
8 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
introductionCalcific aortic valve stenosis (CAVS) is a common disease associated with aging. Oxidative stress participates in the valve calcification process in CAVS. Semicarbazide-sensitive amine oxidase (SSAO), also referred to as vascular adhesion protein 1 (VAP-1), transforms primary amines into aldehydes, generating hydrogen peroxide and ammonia. SSAO is expressed in calcified aortic valves, but its role in valve calcification has remained largely unexplored. The aims of this study were to characterize the expression and the activity of SSAO during aortic valve calcification and to establish the effects of SSAO inhibition on human valvular interstitial cell (VIC) calcification.
methodsHuman aortic valves from
resultsSSAO mRNA, protein, and activity were increased with increasing calcification within human aortic valves and localized in the vicinity of the calcified zones. The valvular SSAO upregulation was consistent after stratification of the subjects according to cardiovascular and CAVS risk factors associated with increased oxidative stress: body mass index, diabetes, and smoking. SSAO mRNA levels were significantly associated with poly(ADP-ribose) polymerase 1 (PARP1) in calcified tissue. Calcification of VIC was inhibited in the presence of the specific SSAO inhibitor LJP1586.
conclusionThe association of SSAO expression and activity with valvular calcification and oxidative stress as well as the decreased VIC calcification by SSAO inhibition points to SSAO as a possible marker and therapeutic target to be further explored in CAVS.
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