ArticleArteriosclerosis, thrombosis, and vascular biology2013
Antioxidant enzymes reduce DNA damage and early activation of valvular interstitial cells in aortic valve sclerosis.
Article in Arteriosclerosis, thrombosis, and vascular biology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 62 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
62 citing papers in PubMed, 105 citations in OpenAlex.
- Extracellular Adenosine Contributes to the Hydrogen Peroxide-Induced Calcification of Cultured Tendon Cells.Current issues in molecular biology · 2026Article
- Characterization of Proteome Features in Patients With Aortic Stenosis Using Data-Independent Acquisition-Based Proteomic Analysis.Korean circulation journal · 2026Article
- Serotonin transporter downregulation is associated with aortic stenosis, and early profibrotic remodeling is mitigated by pharmacological inhibition of HTR2B receptor.Frontiers in cardiovascular medicine · 2026Article
- Inflammation via JAK-STAT/HIF-1α Drives Metabolic Changes in Pentose Phosphate Pathway and Glycolysis That Support Aortic Valve Cell Calcification.Arteriosclerosis, thrombosis, and vascular biology · 2025Article
- Oxidative low-density lipoprotein and shear induced calcification within a calcific aortic valve disease-on-a-chip platform.Frontiers in cardiovascular medicine · 2025Article
- Lysyl Oxidase in Ectopic Cardiovascular Calcification: Role of Oxidative Stress.Antioxidants (Basel, Switzerland) · 2024Article
- Hereditary hemochromatosis with homozygous C282Y HFE mutation: possible clinical model to assess effects of elevated reactive oxygen species on the development of cardiovascular disease.Molecular and cellular biochemistry · 2024Review
- Inhibition of valve mesenchymal stromal cell calcium deposition by bFGF through alternative polyadenylation regulation of the CAT gene.BMC cardiovascular disorders · 2024Article
- The Role of Apoptosis and Oxidative Stress in a Cell Spheroid Model of Calcific Aortic Valve Disease.Cells · 2023Article
- Niclosamide Inhibits Aortic Valve Interstitial Cell Calcification by Interfering with the GSK-3β/β-Catenin Signaling Pathway.Biomolecules & therapeutics · 2023Article
- Targeted inhibition of PTPN22 is a novel approach to alleviate osteogenic responses in aortic valve interstitial cells and aortic valve lesions in mice.BMC medicine · 2023Article
- Hypoxia-inducible factor activation promotes osteogenic transition of valve interstitial cells and accelerates aortic valve calcification in a mice model of chronic kidney disease.Frontiers in cardiovascular medicine · 2023Article
- Mitochondrial Dysfunction and Oxidative Stress in Hereditary Ectopic Calcification Diseases.International journal of molecular sciences · 2022Review
- Enduring Reactive Oxygen Species Emission Causes Aberrant Protein S-Glutathionylation Transitioning Human Aortic Valve Cells from a Sclerotic to a Stenotic Phenotype.Antioxidants & redox signaling · 2022Article
- Review
- Celastrol: A Promising Agent Fighting against Cardiovascular Diseases.Antioxidants (Basel, Switzerland) · 2022Review
- Oxidative Stress in Calcific Aortic Valve Stenosis: Protective Role of Natural Antioxidants.Antioxidants (Basel, Switzerland) · 2022Review
- The Haemodynamic and Pathophysiological Mechanisms of Calcific Aortic Valve Disease.Biomedicines · 2022Review
- Role of oxidative stress in calcific aortic valve disease and its therapeutic implications.Cardiovascular research · 2022Review
- MicroRNA-22 promoted osteogenic differentiation of valvular interstitial cells by inhibiting CAB39 expression during aortic valve calcification.Cellular and molecular life sciences : CMLS · 2022Article
2 more citing papers are in PubMed but not listed here.
Corrections and comments
- Erratum issued
Authors and funding
11 authors at 4 institutions in 2 countries.
Funding
Abstract
objectiveAccumulation of reactive oxygen species (ROS) and remodeling of the microstructure of the cusp characterize aortic valve sclerosis, the early phase of calcific aortic valve disease. These events are associated with activation of valvular interstitial cells (VICs) toward an osteogenic-like phenotype. Because ROS cause DNA damage and transcriptional activation we investigated the relationship between ROS, DNA damage response, and transdifferentiation of VICs. METHODS AND
resultsHuman aortic valve cusps and patient-matched VICs were collected from 39 patients both with and without calcific aortic valve disease. VICs were exposed to hydrogen peroxide (0.1-1 mmol/L) after cell transduction with extracellular superoxide dismutase/catalase adenoviruses and characterized for DNA-damage response, osteogenic transdifferentiation, and calcification. ROS induce relocalization of phosphorylated γH2AX, MRE11, and XRCC1 proteins with expression of osteogenic signaling molecule RUNX2 via AKT. We report a sustained activation of γH2AX in aortic valve sclerosis-derived VICs suggesting their impaired ability to repair DNA damage. Adenovirus superoxide dismutase/catalase transduction decreases ROS-induced DNA damage and VIC transdifferentiation in aortic valve sclerosis-derived cells. Finally, adenoviral transduction with catalase reverts ROS-mediated calcification and cellular transdifferentiation.
conclusionsWe conclude that the ROS-induced DNA damage response is dysfunctional in early asymptomatic stages of calcific aortic valve disease. We unveiled an association among ROS, DNA-damage response, and cellular transdifferentiation, reversible by antioxidant enzymes delivery.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.