ReviewFrontiers in physiology2018
Toll-Like Receptors, Inflammation, and Calcific Aortic Valve Disease.
Review in Frontiers in physiology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 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.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
45 citing papers in PubMed, 62 citations in OpenAlex.
- Orthopedic surgery changes aortic valve composition inAtherosclerosis plus · 2026Article
- KLF5 Downregulation Links Impaired BNIP3-Mediated Mitophagy to Inflammatory Valve Remodeling in Calcific Aortic Valve Disease.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- IL-17-associated Pro-inflammatory Programs in Aortic Valve Interstitial Cell Osteogenic Differentiation: JUN as a Candidate Regulator.Inflammation · 2026Article
- Identification of mitochondria-related genes in calcific aortic valve disease by integrated analysis of single-cell and bulk transcriptomic atlases.Journal of physiology and biochemistry · 2026Article
- Review
- Metabolic Drivers of Valve Calcification and Atrial Remodeling in Calcific Aortic Stenosis.Biomolecules · 2026Review
- Age-associated methionine sulfoxide reductase A protects against valvular interstitial cell senescence and valvular calcification.GeroScience · 2026Article
- Adenosine and ATP differentially control osteogenic gene expression patterns in a cardiac valve cell line.Cardiology journal · 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
- Macrophages as key modulators of calcific aortic valve disease.Frontiers in cardiovascular medicine · 2025Review
- Multiomics identification of ALDH9A1 as a crucial immunoregulatory molecule involved in calcific aortic valve disease.Scientific reports · 2024Article
- Review
- TRPM4 mRNA stabilization by METTL3-mediated m6A modification promotes calcific aortic valve inflammation.Heliyon · 2024Article
- Identification of Circulating Inflammatory Proteins Associated with Calcific Aortic Valve Stenosis by Multiplex Analysis.Cardiovascular toxicology · 2024Observational
- Palmdelphin Deficiency Evokes NF-κB Signaling in Valvular Endothelial Cells and Aggravates Aortic Valvular Remodeling.JACC. Basic to translational science · 2023Article
- Sam68 promotes osteogenic differentiation of aortic valvular interstitial cells by TNF-α/STAT3/autophagy axis.Journal of cell communication and signaling · 2023Article
- Recombinant IL-37 Exerts an Anti-inflammatory Effect on Human Aortic Valve Interstitial Cells through Extracellular and Intracellular Actions.International journal of biological sciences · 2023Article
- Hesperetin, a Promising Dietary Supplement for Preventing the Development of Calcific Aortic Valve Disease.Antioxidants (Basel, Switzerland) · 2022Article
- Interleukin 38 alleviates aortic valve calcification by inhibition of NLRP3.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- Monocytes augment inflammatory responses in human aortic valve interstitial cells via βInflammation research : official journal of the European Histamine Research Society ... [et al.] · 2022Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Inflammation, the primary response of innate immunity, is essential to initiate the calcification process underlying calcific aortic valve disease (CAVD), the most prevalent valvulopathy in Western countries. The pathogenesis of CAVD is multifactorial and includes inflammation, hemodynamic factors, fibrosis, and active calcification. In the development of CAVD, both innate and adaptive immune responses are activated, and accumulating evidences show the central role of inflammation in the initiation and propagation phases of the disease, being the function of Toll-like receptors (TLR) particularly relevant. These receptors act as sentinels of the innate immune system by recognizing pattern molecules from both pathogens and host-derived molecules released after tissue damage. TLR mediate inflammation via NF-κB routes within and beyond the immune system, and play a crucial role in the control of infection and the maintenance of tissue homeostasis. This review outlines the current notions about the association between TLR signaling and the ensuing development of inflammation and fibrocalcific remodeling in the pathogenesis of CAVD. Recent data provide new insights into the inflammatory and osteogenic responses underlying the disease and further support the hypothesis that inflammation plays a mechanistic role in the initiation and progression of CAVD. These findings make TLR signaling a potential target for therapeutic intervention in CAVD.
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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.