ArticleArteriosclerosis, thrombosis, and vascular biology2020
NFκB (Nuclear Factor κ-Light-Chain Enhancer of Activated B Cells) Activity Regulates Cell-Type-Specific and Context-Specific Susceptibility to Calcification in the Aortic Valve.
Article in Arteriosclerosis, thrombosis, and vascular biology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed, 42 citations in OpenAlex.
- Emerging Role of Sodium-Glucose Cotransporter-2 Inhibitors in Aortic Stenosis.JACC. Basic to translational science · 2026Review
- Single-nucleus and machine-learning integration identifies HLA-DRA and FTL as immune-metabolic axes and traditional Chinese medicine-targetable hubs in calcific aortic valve disease.Journal of computer-aided molecular design · 2026Article
- Age-associated methionine sulfoxide reductase A protects against valvular interstitial cell senescence and valvular calcification.GeroScience · 2026Article
- Clinical and Transcriptomic Characteristics of Aortic Stenosis in Patients Undergoing Haemodialysis.Interdisciplinary cardiovascular and thoracic surgery · 2026Article
- Why Are Internal Mammary (Thoracic) Arteries Less Prone to Developing Atherosclerosis Compared to Coronary Arteries? Do Gut Microbiota Play a Role? A Narrative Review.International journal of molecular sciences · 2025Review
- Effects of Cytokines (or Activating Factors) on Arterial Endothelial Cells.International journal of molecular sciences · 2025Review
- Butyrate Produced by Gut Microbiota Regulates Atherosclerosis: A Narrative Review of the Latest Findings.International journal of molecular sciences · 2025Review
- Modulation of mechanosensitive genes during embryonic aortic arch development.Developmental dynamics : an official publication of the American Association of Anatomists · 2025Article
- Effect of Glucagon-like Peptide-1 Receptor Agonism on Aortic Valve Stenosis Risk: A Mendelian Randomization Analysis.Journal of clinical medicine · 2024Article
- Integrated machine learning and Mendelian randomization reveal PALMD as a prognostic biomarker for nonspecific orbital inflammation.Scientific reports · 2024Article
- Biomechanical Remodeling of Aortic Valve Interstitial Cells During Calcified Lesion Formation In Vitro.Annals of biomedical engineering · 2024Article
- Identification of Diagnostic Genes of Aortic Stenosis That Progresses from Aortic Valve Sclerosis.Journal of inflammation research · 2024Article
- Environmental epigenetics and the loneliness epidemic.Environmental epigenetics · 2024Article
- Identification and validation of the diagnostic biomarker MFAP5 for CAVD with type 2 diabetes by bioinformatics analysis.Frontiers in immunology · 2024Article
- Palmdelphin Deficiency Evokes NF-κB Signaling in Valvular Endothelial Cells and Aggravates Aortic Valvular Remodeling.JACC. Basic to translational science · 2023Article
- Liraglutide Attenuates Aortic Valve Calcification in a High-Cholesterol-Diet-Induced Experimental Calcific Aortic Valve Disease Model in Apolipoprotein E-Deficient Mice.Journal of cardiovascular development and disease · 2023Article
- CD163+ macrophages restrain vascular calcification, promoting the development of high-risk plaque.JCI insight · 2023Article
- Endothelial-to-mesenchymal transition: An underappreciated mediator of diabetic complications.Frontiers in endocrinology · 2023Review
- PALMD regulates aortic valve calcification via altered glycolysis and NF-κB-mediated inflammation.The Journal of biological chemistry · 2022Article
- Review
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
objectiveAlthough often studied independently, little is known about how aortic valve endothelial cells and valve interstitial cells interact collaborate to maintain tissue homeostasis or drive valve calcific pathogenesis. Inflammatory signaling is a recognized initiator of valve calcification, but the cell-type-specific downstream mechanisms have not been elucidated. In this study, we test how inflammatory signaling via NFκB (nuclear factor κ-light-chain enhancer of activated B cells) activity coordinates unique and shared mechanisms of valve endothelial cells and valve interstitial cells differentiation during calcific progression. Approach and Results: Activated NFκB was present throughout the calcific aortic valve disease (CAVD) process in both endothelial and interstitial cell populations in an established mouse model of hypercholesterolemia-induced CAVD and in human CAVD. NFκB activity induces endothelial to mesenchymal transformation in 3-dimensional cultured aortic valve endothelial cells and subsequent osteogenic calcification of transformed cells. Similarly, 3-dimensional cultured valve interstitial cells calcified via NFκB-mediated osteogenic differentiation. NFκB-mediated endothelial to mesenchymal transformation was directly demonstrated in vivo during CAVD via genetic lineage tracking. Genetic deletion of NFκB in either whole valves or valve endothelium only was sufficient to prevent valve-specific molecular and cellular mechanisms of CAVD in vivo despite the persistence of a CAVD inducing environment.
conclusionsOur results identify NFκB signaling as an essential molecular regulator for both valve endothelial and interstitial participation in CAVD pathogenesis. Direct demonstration of valve endothelial cell endothelial to mesenchymal transformation transmigration in vivo during CAVD highlights a new cellular population for further investigation in CAVD morbidity. The efficacy of valve-specific NFκB modulation in inhibiting hypercholesterolemic CAVD suggests potential benefits of multicell type integrated investigation for biological therapeutic development and evaluation for CAVD.
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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.