ReviewJournal of cardiovascular translational research2016
Calcific Aortic Valve Disease: Part 1--Molecular Pathogenetic Aspects, Hemodynamics, and Adaptive Feedbacks.
Review in Journal of cardiovascular translational research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
24 citing papers in PubMed.
- Shared Risk Factors and Molecular Mechanisms Between Aortic Stenosis and Atherosclerosis: A Rationale for Therapeutic Repositioning.International journal of molecular sciences · 2025Review
- Aortic valve calcification in echocardiography is a prognostic factor for short-term adverse outcomes in elderly patients with severe COVID-19: a retrospective cohort study.Journal of thoracic disease · 2025Article
- Advances in Pathophysiological Mechanisms of Degenerative Aortic Valve Disease.Cardiology research · 2025Review
- Nuclear magnetic resonance spectroscopy to quantify major extracellular matrix components in fibro-calcific aortic valve disease.Scientific reports · 2023Article
- Native bicuspid aortic valve thrombus in a patient with an ascending aorta aneurysm: A case report.Heliyon · 2023Article
- CircRNA/lncRNA-miRNA-mRNA network and gene landscape in calcific aortic valve disease.BMC genomics · 2023Article
- Article
- Adding a "Notch" to Cardiovascular Disease Therapeutics: A MicroRNA-Based Approach.Frontiers in cell and developmental biology · 2021Review
- Pathogenesis and Molecular Immune Mechanism of Calcified Aortic Valve Disease.Frontiers in cardiovascular medicine · 2021Review
- Clinical-pathological correlations of BAV and the attendant thoracic aortopathies. Part 1: Pluridisciplinary perspective on their hemodynamics and morphomechanics.Journal of molecular and cellular cardiology · 2019Article
- Clinical-pathological correlations of BAV and the attendant thoracic aortopathies. Part 2: Pluridisciplinary perspective on their genetic and molecular origins.Journal of molecular and cellular cardiology · 2019Review
- Biofunctionalization of decellularized porcine aortic valve with OPG-loaded PCL nanoparticles for anti-calcification.RSC advances · 2019Article
- Increased Expression of miR-146a in Valvular Tissue From Patients With Aortic Valve Stenosis.Frontiers in cardiovascular medicine · 2019Article
- Morphomechanic phenotypic variability of sarcomeric cardiomyopathies: A multifactorial polygenic perspective.Journal of molecular and cellular cardiology · 2019Review
- Simvastatin reduces the TLR4-induced inflammatory response in human aortic valve interstitial cells.The Journal of surgical research · 2018Article
- The new era of whole-exome sequencing in congenital heart disease: brand-new insights into rare pathogenic variants.Journal of thoracic disease · 2018Article
- Challenges and Controversies in Hypertrophic Cardiomyopathy: Clinical, Genomic and Basic Science Perspectives.Revista espanola de cardiologia (English ed.) · 2018Article
- Implementing genome-driven personalized cardiology in clinical practice.Journal of molecular and cellular cardiology · 2018Review
- Know Me! Unraveling the Riddle of Calcific Aortic Valve Disease by Bioinformatics.The Tohoku journal of experimental medicine · 2017Article
- High mobility group box 1 induces calcification of aortic valve interstitial cells via toll-like receptor 4.Molecular medicine reports · 2017Article
Corrections and comments
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Authors and funding
1 author.
Funding
Abstract
Aortic valvular stenosis (AVS), produced by calcific aortic valve disease (CAVD) causing reduced cusp opening, afflicts mostly older persons eventually requiring valve replacement. CAVD had been considered "degenerative," but newer investigations implicate active mechanisms similar to atherogenesis--genetic predisposition and signaling pathways, lipoprotein deposits, chronic inflammation, and calcification/osteogenesis. Consequently, CAVD may eventually be controlled/reversed by lifestyle and pharmacogenomics remedies. Its management should be comprehensive, embracing not only the valve but also the left ventricle and the arterial system with their interdependent morphomechanics/hemodynamics, which underlie the ensuing diastolic and systolic LV dysfunction. Compared to even a couple of decades ago, we now have an increased appreciation of genomic and cytomolecular pathogenetic mechanisms underlying CAVD. Future pluridisciplinary studies will characterize better and more completely its pathobiology, evolution, and overall dynamics, encompassing intricate feedback processes involving specific signaling molecules and gene network cascades. They will herald more effective, personalized medicine treatments of CAVD/AVS.
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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.