ReviewCurrent cardiology reviews2018
Cellular Mechanisms of Valvular Thickening in Early and Intermediate Calcific Aortic Valve Disease.
Review in Current cardiology reviews, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 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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Who cites it
21 citing papers in PubMed, 30 citations in OpenAlex.
- Correlation Between Plasma Matrix Metalloproteinase-28 Levels and Severity of Calcific Aortic Valve Stenosis.Medical science monitor : international medical journal of experimental and clinical research · 2020Trial
- Circulating CTRP9 and aortic valve calcification jointly predict coronary artery calcification in coronary heart disease patients.Frontiers in nutrition · 2026Article
- Trimethylamine-N-oxide promotes fibrotic activation of quiescent valvular interstitial cells via endoplasmic reticulum stress.Scientific reports · 2025Article
- The Heart's Small Molecules: The Importance of MicroRNAs in Cardiovascular Health.Journal of clinical medicine · 2025Review
- Mechanistic Insights into Bioprosthetic Heart Valve Calcification and Anti-Calcification Strategies.Reviews in cardiovascular medicine · 2025Review
- Immunometabolism in the Aging Heart.Journal of the American Heart Association · 2025Review
- Long-term all-cause death prediction by coronary, aortic, and valvular calcification in patients with acute ST-segment elevation myocardial infarction.BMC cardiovascular disorders · 2024Article
- Challenges of aortic valve tissue culture - maintenance of viability and extracellular matrix in the pulsatile dynamic microphysiological system.Journal of biological engineering · 2023Article
- Exploration and validation of the influence of angiogenesis-related factors in aortic valve calcification.Frontiers in cardiovascular medicine · 2023Article
- Activation of AcvR1-Mediated Signaling Results in Semilunar Valve Defects.Journal of cardiovascular development and disease · 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
- Pro-inflammatory mediators released by activated monocytes promote aortic valve fibrocalcific activity.Molecular medicine (Cambridge, Mass.) · 2022Article
- Shared gene characteristics and molecular mechanisms of macrophages M1 polarization in calcified aortic valve disease.Frontiers in cardiovascular medicine · 2022Article
- Serotonin-A Driver of Progressive Heart Valve Disease.Frontiers in cardiovascular medicine · 2022Review
- Local Renin-Angiotensin System Signaling Mediates Cellular Function of Aortic Valves.Annals of biomedical engineering · 2021Article
- LncRNA ANRIL acts as a modular scaffold of WDR5 and HDAC3 complexes and promotes alteration of the vascular smooth muscle cell phenotype.Cell death & disease · 2020Article
- Endothelial-to-Mesenchymal Transition in Calcific Aortic Valve Disease.Acta Cardiologica Sinica · 2020Review
- TLR4 Stimulation Promotes Human AVIC Fibrogenic Activity through Upregulation of Neurotrophin 3 Production.International journal of molecular sciences · 2020Article
- Article
- Oscillatory fluid-induced mechanobiology in heart valves with parallels to the vasculature.Vascular biology (Bristol, England) · 2020Review
Corrections and comments
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Authors and funding
3 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundCalcific aortic valve disease is common in an aging population. It is an active atheroinflammatory process that has an initial pathophysiology and similar risk factors as atherosclerosis. However, the ultimate disease phenotypes are markedly different. While coronary heart disease results in rupture-prone plaques, calcific aortic valve disease leads to heavily calcified and ossified valves. Both are initiated by the retention of low-density lipoprotein particles in the subendothelial matrix leading to sterile inflammation. In calcific aortic valve disease, the process towards calcification and ossification is preceded by valvular thickening, which can cause the first clinical symptoms. This is attributable to the accumulation of lipids, inflammatory cells and subsequently disturbances in the valvular extracellular matrix. Fibrosis is also increased but the innermost extracellular matrix layer is simultaneously loosened. Ultimately, the pathological changes in the valve cause massive calcification and bone formation - the main reasons for the loss of valvular function and the subsequent myocardial pathology.
conclusionCalcification may be irreversible, and no drug treatments have been found to be effective, thus it is imperative to emphasize lifestyle prevention of the disease. Here we review the mechanisms underpinning the early stages of the disease.
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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.