ArticleJournal of molecular histology2020
Lipid mass spectrometry imaging and proteomic analysis of severe aortic stenosis.
Article in Journal of molecular histology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
What it found
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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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Who cites it
14 citing papers in PubMed, 23 citations in OpenAlex.
- Complement Activation by Post-Translationally Modified Proteins: Links to Chronic Inflammation and Autoimmunity.Immunological reviews · 2026Review
- Complement Component C4B Prioritization Through Drug‒Target Mendelian Randomization and Proteomic Analysis Reveals a Novel Therapeutic Target for Calcific Aortic Valve Stenosis.Cardiovascular drugs and therapy · 2026Article
- Serum Lipidomic Profile Signature of Active Acromegaly and Relationships to Cardiovascular Disease.International journal of molecular sciences · 2026Article
- Integrated multiomics of pressure overload in the human heart prioritizes targets relevant to heart failure.Nature communications · 2025Article
- Atherosclerosis, calcific aortic valve disease and mitral annular calcification: same or different?International journal of cardiology · 2025Review
- Mass Spectrometry Imaging of Two Neocortical Areas Reveals the Histological Selectivity of Schizophrenia-Associated Lipid Alterations.Consortium psychiatricum · 2024Article
- New insight of complement system in the process of vascular calcification.Journal of cellular and molecular medicine · 2023Review
- Biomineralogical signatures of breast microcalcifications.Science advances · 2023Article
- Lipid Changes in the Peri-Implantation Period with Mass Spectrometry Imaging: A Systematic Review.Life (Basel, Switzerland) · 2023Review
- Lipoproteins and Calcific Aortic Valve Disease: Hardening Evidence?Arteriosclerosis, thrombosis, and vascular biology · 2022Article
- High-Density Lipoprotein and Long-Term Incidence and Progression of Aortic Valve Calcification: The Multi-Ethnic Study of Atherosclerosis.Arteriosclerosis, thrombosis, and vascular biology · 2022Article
- Measures of high-density lipoprotein function in men and women with severe aortic stenosis.Lipids in health and disease · 2022Article
- Perspectives on pediatric congenital aortic valve stenosis: Extracellular matrix proteins, post translational modifications, and proteomic strategies.Frontiers in cardiovascular medicine · 2022Review
- Multi-omics ofFrontiers in cardiovascular medicine · 2022Article
Corrections and comments
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Authors and funding
7 authors at 4 institutions in 2 countries.
Funding
Abstract
Severe aortic stenosis (AS) is prevalent in adults ≥ 65 years, a significant cause of morbidity and mortality, with no medical therapy. Lipid and proteomic alterations of human AS tissue were determined using mass spectrometry imaging (MSI) and liquid chromatography electrospray ionization tandem mass spectrometry (LC-ESI-MS/MS) to understand histopathology, potential biomarkers of disease, and progression from non-calcified to calcified phenotype. A reproducible MSI method was developed using healthy murine aortic valves (n = 3) and subsequently applied to human AS (n = 2). Relative lipid levels were spatially mapped and associated with different microdomains. Proteomics for non-calcified and calcified microdomains were performed to ascertain differences in expression. Increased pro-osteogenic and inflammatory lysophosphatidylcholine (LPC) 16:0 and 18:0 were co-localized with calcified microdomains. Proteomics analysis identified differential patterns in calcified microdomains with high LPC and low cholesterol as compared to non-calcified microdomains with low LPC and high cholesterol. Calcified microdomains had higher levels of: apolipoproteins (Apo) B-100 (p < 0.001) and Apo A-IV (p < 0.001), complement C3 and C4-B (p < 0.001), C5 (p = 0.007), C8 beta chain (p = 0.013) and C9 (p = 0.010), antithrombotic proteins alpha-2-macroglobulin (p < 0.0001) and antithrombin III (p = 0.002), and higher anti-calcific fetuin-A (p = 0.02), while the osteoblast differentiating factor transgelin (p < 0.0001), extracellular matrix proteins versican, prolargin, and lumican ( p < 0.001) and regulator protein complement factor H (p < 0.001) were higher in non-calcified microdomains. A combined lipidomic and proteomic approach provided insight into factors potentially contributing to progression from non-calcified to calcific disease in severe AS. Additional studies of these candidates and protein networks could yield new targets for slowing progression of AS.
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