ReviewJournal of cardiovascular translational research2016
Calcific Aortic Valve Disease: Part 2-Morphomechanical Abnormalities, Gene Reexpression, and Gender Effects on Ventricular Hypertrophy and Its Reversibility.
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 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.
- Cardiac magnetic resonance patterns of left ventricular remodeling in patients with severe aortic stenosis referred to surgical aortic valve replacement.Scientific reports · 2024Article
- Prioritization of Candidate Biomarkers for Degenerative Aortic Stenosis through a Systems Biology-Based In-Silico Approach.Journal of personalized medicine · 2022Article
- Impact of Decreased Transmural Conduction Velocity on the Function of the Human Left Ventricle: A Simulation Study.BioMed research international · 2020Article
- Association Between Serum Leptin Level and Calcific Aortic Valve Disease.Journal of the American Heart Association · 2019Article
- 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
- 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
- Eplerenone pretreatment protects the myocardium against ischaemia/reperfusion injury through the phosphatidylinositol 3-kinase/Akt-dependent pathway in diabetic rats.Molecular and cellular biochemistry · 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
- Genomic translational research: Paving the way to individualized cardiac functional analyses and personalized cardiology.International journal of cardiology · 2017Review
Corrections and comments
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Authors and funding
1 author.
Funding
Abstract
In part 1, we considered cytomolecular mechanisms underlying calcific aortic valve disease (CAVD), hemodynamics, and adaptive feedbacks controlling pathological left ventricular hypertrophy provoked by ensuing aortic valvular stenosis (AVS). In part 2, we survey diverse signal transduction pathways that precede cellular/molecular mechanisms controlling hypertrophic gene expression by activation of specific transcription factors that induce sarcomere replication in-parallel. Such signaling pathways represent potential targets for therapeutic intervention and prevention of decompensation/failure. Hypertrophy provoking signals, in the form of dynamic stresses and ligand/effector molecules that bind to specific receptors to initiate the hypertrophy, are transcribed across the sarcolemma by several second messengers. They comprise intricate feedback mechanisms involving gene network cascades, specific signaling molecules encompassing G protein-coupled receptors and mechanotransducers, and myocardial stresses. Future multidisciplinary studies will characterize the adaptive/maladaptive nature of the AVS-induced hypertrophy, its gender- and individual patient-dependent peculiarities, and its response to surgical/medical interventions. They will herald more effective, precision medicine treatments.
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Registered trials
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