ReviewCells2022
Cellular Senescence, Aging and Non-Aging Processes in Calcified Aortic Valve Stenosis: From Bench-Side to Bedside.
Review in Cells, 2022. 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.
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
14 citing papers in PubMed, 19 citations in OpenAlex.
- Involvement of TGF-β, mTOR, and inflammatory mediators in aging alterations during myxomatous mitral valve disease in a canine model.GeroScience · 2025Review
- Impact of smoking on cardiovascular health: Mechanisms, epidemiology and specific concerns regarding congenital heart disease.International journal of cardiology. Congenital heart disease · 2025Review
- Telomere Length and Clonal Hematopoiesis of Indeterminate Potential: A Loop Between Two Key Players in Aortic Valve Disease?Journal of cardiovascular development and disease · 2025Review
- [The association between biological aging markers and valvular heart diseases].Zhejiang da xue xue bao. Yi xue ban = Journal of Zhejiang University. Medical sciences · 2025Article
- Initiation of transthyretin aggregation at neutral pH by fluid agitation.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Bibliometric analysis of treatment modalities in calcific aortic valve stenosis.Frontiers in pharmacology · 2025Article
- Aggregation of Transthyretin by Fluid Agitation.bioRxiv : the preprint server for biology · 2024Article
- Mast cells: a novel therapeutic avenue for cardiovascular diseases?Cardiovascular research · 2024Review
- Morusin Alleviates Aortic Valve Calcification by Inhibiting Valve Interstitial Cell Senescence Through Ccnd1/Trim25/Nrf2 Axis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- Cellular Senescence as a Targetable Risk Factor for Cardiovascular Diseases: Therapeutic Implications:JACC. Basic to translational science · 2024Review
- Epigenetic age acceleration and risk of aortic valve stenosis: a bidirectional Mendelian randomization study.Clinical epigenetics · 2024Article
- Cells in Atherosclerosis: Focus on Cellular Senescence from Basic Science to Clinical Practice.International journal of molecular sciences · 2023Review
- A biomarker framework for cardiac aging: the Aging Biomarker Consortium consensus statement.Life medicine · 2023Article
- A Straightforward Cytometry-Based Protocol for the Comprehensive Analysis of the Inflammatory Valve Infiltrate in Aortic Stenosis.International journal of molecular sciences · 2023Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Aortic valve stenosis (AS) is the most common valvular heart disease. The incidence of AS increases with age, however, a significant proportion of elderly people have no significant AS, indicating that both aging and nonaging pathways are involved in the pathomechanism of AS. Age-related and stress-induced cellular senescence accompanied by further active processes represent the key elements of AS pathomechanism. The early stage of aortic valve degeneration involves dysfunction and disruption of the valvular endothelium due to cellular senescence and mechanical stress on blood flow. These cells are replaced by circulating progenitor cells, but in an age-dependent decelerating manner. When endothelial denudation is no longer replaced by progenitor cells, the path opens for focal lipid deposition, initiating subsequent oxidation, inflammation and micromineralisation. Later stages of AS feature a complex active process with extracellular matrix remodeling, fibrosis and calcification. Echocardiography is the gold standard method for diagnosing aortic valve disease, although computed tomography and cardiac magnetic resonance are useful additional imaging methods. To date, no medical treatment has been proven to halt the progression of AS. Elucidation of differences and similarities between vascular and valvular calcification pathomechanisms may help to find effective medical therapy and reduce the increasing health burden 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.