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Calcific Aortic Valve Disease and Aortic Stenosis

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A special issue of Biomedicines (ISSN 2227-9059). This special issue belongs to the section "Molecular and Translational Medicine".

Deadline for manuscript submissions: closed (30 November 2021) | Viewed by 14523

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Special Issue Editor

Dr. Andreas Weber

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Guest Editor

Department of Heart Surgery, Heinrich-Heine-University, Duesseldorf, Germany
Interests: aortic valve stenosis and calcific aortic valve disease; extracellular vesicles in cardiovascular diseases; endothelial to mesenchymal transition of vascular endothelial cells; purinergic signaling; 3D-cell culture and tissue culture models

Special Issue Information

Dear Colleagues,

This Special Issue, “Calcific Aortic Valve Disease and Aortic Stenosis”, will mainly focus on novel insights into the key mechanisms underlying calcific aortic valve disease (CAVD).

CAVD is as a slow and progressive (but also an active and regulated) process involving the creation of calcium nodules, lipoprotein accumulation, and chronic inflammation. Despite substantial progress in recent years, there is still no solid evidence that the progression of CAVD can be prevented with any medical treatment, and consequently, aortic valve replacement (AVR) remains the gold standard for the treatment of symptomatic aortic stenosis (AS).

We cordially invite authors in the field to submit original research or review articles pertaining to this important and rapidly progressing field. Potential topics include, but are not limited to:

Novel basic mechanisms in the initiation and progression of CAVD;
Biomarkers in CAVD;
Cardiac regeneration;
Myofibroblastic and osteogenic differentiation of valvular interstitial cells (VICs);
Extracellular matrix (ECM) signaling and remodeling in CAVD;
Novel in-vivo and in-vitro models to investigate basic mechanisms in CAVD;
Functionality and plasticity of valvular endothelial cells (VECs);
Endothelial-to-mesenchymal transition;
Role of extracellular vesicles (EVs) in the pathogenesis of CAVD;
Therapeutic approaches to preventing CAVD progression.

Dr. Andreas Weber
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Biomedicines is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2600 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

calcific aortic valve disease
calcification
biomineralization
extracellular vesicles
extracellular matrix remodeling
endothelial-to-mesenchymal transition
osteogenic differentiation

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Published Papers (4 papers)

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Research

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17 pages, 5820 KiB

Open AccessArticle

Reproducible In Vitro Tissue Culture Model to Study Basic Mechanisms of Calcific Aortic Valve Disease: Comparative Analysis to Valvular Interstitials Cells

by Andreas Weber, Melissa Pfaff, Friederike Schöttler, Vera Schmidt, Artur Lichtenberg and Payam Akhyari

Biomedicines 2021, 9(5), 474; https://doi.org/10.3390/biomedicines9050474 - 26 Apr 2021

Cited by 11 | Viewed by 3303

Abstract

The hallmarks of calcific aortic valve disease (CAVD), an active and regulated process involving the creation of calcium nodules, lipoprotein accumulation, and chronic inflammation, are the significant changes that occur in the composition, organization, and mechanical properties of the extracellular matrix (ECM) of the aortic valve (AV). Most research regarding CAVD is based on experiments using two-dimensional (2D) cell culture or artificially created three-dimensional (3D) environments of valvular interstitial cells (VICs). Because the valvular ECM has a powerful influence in regulating pathological events, we developed an in vitro AV tissue culture model, which is more closely able to mimic natural conditions to study cellular responses underlying CAVD. AV leaflets, isolated from the hearts of 6–8-month-old sheep, were fixed with needles on silicon rubber rings to achieve passive tension and treated in vitro under pro-degenerative and pro-calcifying conditions. The degeneration of AV leaflets progressed over time, commencing with the first visible calcified domains after 14 d and winding up with the distinct formation of calcium nodules, heightened stiffness, and clear disruption of the ECM after 56 d. Both the expression of pro-degenerative genes and the myofibroblastic differentiation of VICs were altered in AV leaflets compared to that in VIC cultures. In this study, we have established an easily applicable, reproducible, and cost-effective in vitro AV tissue culture model to study pathological mechanisms underlying CAVD. The valvular ECM and realistic VIC–VEC interactions mimic natural conditions more closely than VIC cultures or 3D environments. The application of various culture conditions enables the examination of different pathological mechanisms underlying CAVD and could lead to a better understanding of the molecular mechanisms that lead to VIC degeneration and AS. Our model provides a valuable tool to study the complex pathobiology of CAVD and can be used to identify potential therapeutic targets for slowing disease progression. Full article

(This article belongs to the Special Issue Calcific Aortic Valve Disease and Aortic Stenosis)

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17 pages, 3213 KiB

Open AccessArticle

Heme-Mediated Activation of the Nrf2/HO-1 Axis Attenuates Calcification of Valve Interstitial Cells

by Enikő Balogh, Arpan Chowdhury, Haneen Ababneh, Dávid Máté Csiki, Andrea Tóth and Viktória Jeney

Biomedicines 2021, 9(4), 427; https://doi.org/10.3390/biomedicines9040427 - 15 Apr 2021

Cited by 18 | Viewed by 4485

Abstract

Calcific aortic valve stenosis (CAVS) is a heart disease characterized by the progressive fibro-calcific remodeling of the aortic valves, an actively regulated process with the involvement of the reactive oxygen species-mediated differentiation of valvular interstitial cells (VICs) into osteoblast-like cells. Nuclear factor erythroid 2-related factor 2 (Nrf2) regulates the expression of a variety of antioxidant genes, and plays a protective role in valve calcification. Heme oxygenase-1 (HO-1), an Nrf2-target gene, is upregulated in human calcified aortic valves. Therefore, we investigated the effect of Nrf2/HO-1 axis in VIC calcification. We induced osteogenic differentiation of human VICs with elevated phosphate and calcium-containing osteogenic medium (OM) in the presence of heme. Heme inhibited Ca deposition and OM-induced increase in alkaline phosphatase and osteocalcin (OCN) expression. Heme induced Nrf2 and HO-1 expression in VICs. Heme lost its anti-calcification potential when we blocked transcriptional activity Nrf2 or enzyme activity of HO-1. The heme catabolism products bilirubin, carbon monoxide, and iron, and also ferritin inhibited OM-induced Ca deposition and OCN expression in VICs. This study suggests that heme-mediated activation of the Nrf2/HO-1 pathway inhibits the calcification of VICs. The anti-calcification effect of heme is attributed to the end products of HO-1-catalyzed heme degradation and ferritin. Full article

(This article belongs to the Special Issue Calcific Aortic Valve Disease and Aortic Stenosis)

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8 pages, 841 KiB

Open AccessCommunication

Elements of Immunoglobulin E Network Associate with Aortic Valve Area in Patients with Acquired Aortic Stenosis

by Daniel P. Potaczek, Aleksandra Przytulska-Szczerbik, Stanisława Bazan-Socha, Artur Jurczyszyn, Ko Okumura, Chiharu Nishiyama, Anetta Undas and Ewa Wypasek

Biomedicines 2021, 9(1), 23; https://doi.org/10.3390/biomedicines9010023 - 31 Dec 2020

Cited by 2 | Viewed by 2351

Abstract

Allergic mechanisms are likely involved in atherosclerosis and its clinical presentations, such as coronary artery disease (CAD). It has been previously reported that CAD severity associates with serum levels of immunoglobulin E (IgE), the molecule that, along with its high-affinity receptor (FcԑRI), plays a central role in allergic reactions. Considering multiple pathophysiological similarities between atherosclerosis and acquired aortic (valve) stenosis (AS), we speculated that allergic pathways could also contribute to the AS mechanisms and grading. To validate this hypothesis, we first checked whether total serum IgE levels associate with echocardiographic markers of AS severity. Having found a positive correlation between serum IgE and aortic valve area (AVA), we further speculated that also total IgE-determining genetic polymorphisms in FCER1A, a locus encoding an allergen-biding FcԑRI subunit, are related to acquired AS severity. Indeed, the major allele of rs2251746 polymorphism, known to associate with higher IgE levels, turned out to correlate with larger AVA, a marker of less severe AS. Our findings surprisingly suggest a protective role of IgE pathways against AS progression. IgE-mediated protective mechanisms in AS require further investigations. Full article

(This article belongs to the Special Issue Calcific Aortic Valve Disease and Aortic Stenosis)

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