ArticleBMC cardiovascular disorders2019
Heat shock protein 90 is downregulated in calcific aortic valve disease.
Article in BMC cardiovascular disorders, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 22 citations in OpenAlex.
- Multimodal Analytical Tools to Enhance Mechanistic Understanding of Aortic Valve Calcification.The American journal of pathology · 2024Review
- The Complex Relationship between Hypoxia Signaling, Mitochondrial Dysfunction and Inflammation in Calcific Aortic Valve Disease: Insights from the Molecular Mechanisms to Therapeutic Approaches.International journal of molecular sciences · 2023Review
- Aspirin relieves the calcification of aortic smooth muscle cells by enhancing the heat shock response.Pharmaceutical biology · 2022Article
- Article
- Role of oxidative stress in calcific aortic valve disease and its therapeutic implications.Cardiovascular research · 2022Review
- Pericardial Fluid Annexin A1 Is a Marker of Atrial Fibrillation in Aortic Stenosis: A Proteomics Analysis.Journal of personalized medicine · 2022Article
- Heat Shock Protein 90 as Therapeutic Target for CVDs and Heart Ageing.International journal of molecular sciences · 2022Review
- Models and Techniques to Study Aortic Valve CalcificationFrontiers in pharmacology · 2022Review
- Multi-omics ofFrontiers in cardiovascular medicine · 2022Article
- Label-Free Multiphoton Microscopy for the Detection and Monitoring of Calcific Aortic Valve Disease.Frontiers in cardiovascular medicine · 2021Review
- Age related extracellular matrix and interstitial cell phenotype in pulmonary valves.Scientific reports · 2020Article
- Roles of Histone Acetylation Modifiers and Other Epigenetic Regulators in Vascular Calcification.International journal of molecular sciences · 2020Review
Corrections and comments
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Authors and funding
9 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundCalcific aortic valve disease (CAVD) is an atheroinflammatory process; finally it leads to progressive calcification of the valve. There is no effective pharmacological treatment for CAVD and many of the underlying molecular mechanisms remain unknown. We conducted a proteomic study to reveal novel factors associated with CAVD.
methodsWe compared aortic valves from patients undergoing valvular replacement surgery due to non-calcified aortic insufficiency (control group, n = 5) to a stenotic group (n = 7) using two-dimensional difference gel electrophoresis (2D-DIGE). Protein spots were identified with mass spectrometry. Western blot and immunohistochemistry were used to validate the results in a separate patient cohort and Ingenuity Pathway Analysis (IPA) was exploited to predict the regulatory network of CAVD.
resultsWe detected an upregulation of complement 9 (C9), serum amyloid P-component (APCS) and transgelin as well as downregulation of heat shock protein (HSP90), protein disulfide isomerase A3 (PDIA3), annexin A2 (ANXA2) and galectin-1 in patients with aortic valve stenosis. The decreased protein expression of HSP90 was confirmed with Western blot.
conclusionsWe describe here a novel data set of proteomic changes associated with CAVD, including downregulation of the pro-inflammatory cytosolic protein, HSP90.
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