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Molecular and CelluIar Mechanisms of Valvular Heart Disease
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Molecular and CelluIar Mechanisms of Valvular Heart Disease

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pathology, Diagnostics, and Therapeutics".

Deadline for manuscript submissions: closed (20 November 2024) | Viewed by 5378

Special Issue Editors

Prof. Dr. Evaldas Girdauskas

E-Mail Website
Guest Editor
University Hospital Augsburg, Augsburg, Germany
Interests: heart; valvular heart disease; heart valve disorder; myocardial disease
Prof. Dr. Tanja Zeller

E-Mail Website
Guest Editor
Univbersity Heart & Vascular Center Hamburg, Hamburg, Germany
Interests: translational biomarkers; cardiovascular disease; molecular mechanisms; systems medicine
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

The understanding of the pathophysiology of heart diseases has undergone major advances over the last decades. In line with the raising expertise in molecular cardiology and the improvement of clinical imaging modalities, several key cellular and molecular pathways leading to specific types of heart disease have been identified. This Special Issue is specifically dedicated to the novel molecular and cellular mechanisms leading to valvular heart disease (VHD). Two major topics are intended to be covered by this collection: the development of degenerative heart valve disease, and the pathophysiology of valvular cardiomyopathy (i.e., cardiomyopathy as a sequel of heart valve dysfunction). Mechanisms leading to heart valve degeneration—genetical, environmental, metabolic, and hemodynamic factors—are intended to be addressed in the first part of this Special Issue. The focus will be on emerging clinical implications, including novel biomarkers and potential innovative treatment targets. Valvular cardiomyopathy is an underestimated and underdiagnosed clinical entity that summarizes myocardial damage as a sequel of heart valve disease. Specific molecular pathways have recently been reported in different types of valvular cardiomyopathy (e.g., valvular stenosis vs. regurgitation) and should be specifically covered by the second part of this Special Issue. Different mechanisms leading to myocardial damage due to specific valvular dysfunction may lead to a differential response to treatment and be associated with variable prognosis. We welcome original research articles, systematic reviews and meta-analyses, as well as selected case reports/case series dealing with the abovementioned topics. Furthermore, well-designed prospective study protocols will be similarly considered.                        

We look forward to receiving your contributions.

Prof. Dr. Evaldas Girdauskas
Prof. Dr. Tanja Zeller
Guest Editors

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. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. 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

  • heart disease
  • valvular heart disease
  • heart valve disorder
  • aortic valve disease
  • mitral valve disease
  • valvular cardiomyopathy
  • myocardial disease
  • valvular regurgitation
  • valvular stenosis
  • myocardial fibrosis

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Published Papers (3 papers)

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Research

17 pages, 2124 KiB  
Article
Monoamine Oxidase Contributes to Valvular Oxidative Stress: A Prospective Observational Pilot Study in Patients with Severe Mitral Regurgitation
by Raluca Șoșdean, Maria D. Dănilă, Loredana N. Ionică, Alexandru S. Pescariu, Monica Mircea, Adina Ionac, Cristian Mornoș, Constantin T. Luca, Horea B. Feier, Danina M. Muntean and Adrian Sturza
Int. J. Mol. Sci. 2024, 25(19), 10307; https://doi.org/10.3390/ijms251910307 - 25 Sep 2024
Cited by 2 | Viewed by 1251
Abstract
Monoamine oxidases (MAOs), mitochondrial enzymes that constantly produce hydrogen peroxide (H2O2) as a byproduct of their activity, have been recently acknowledged as contributors to oxidative stress in cardiometabolic pathologies. The present study aimed to assess whether MAOs are mediators [...] Read more.
Monoamine oxidases (MAOs), mitochondrial enzymes that constantly produce hydrogen peroxide (H2O2) as a byproduct of their activity, have been recently acknowledged as contributors to oxidative stress in cardiometabolic pathologies. The present study aimed to assess whether MAOs are mediators of valvular oxidative stress and interact in vitro with angiotensin 2 (ANG2) to mimic the activation of the renin–angiotensin system. To this aim, valvular tissue samples were harvested from 30 patients diagnosed with severe primary mitral regurgitation and indication for surgical repair. Their reactive oxygen species (ROS) levels were assessed by means of a ferrous oxidation xylenol orange (FOX) assay, while MAO expression was assessed by immune fluorescence (protein) and qRT-PCR (mRNA). The experiments were performed using native valvular tissue acutely incubated or not with angiotensin 2 (ANG2), MAO inhibitors (MAOI) and the angiotensin receptor blocker, irbesartan (Irb). Correlations between oxidative stress and echocardiographic parameters were also analyzed. Ex vivo incubation with ANG2 increased MAO-A and -B expression and ROS generation. The level of valvular oxidative stress was negatively correlated with the left ventricular ejection fraction. MAOI and Irb reduced valvular H2O2. production. In conclusion, both MAO isoforms are expressed in pathological human mitral valves and contribute to local oxidative stress and ventricular functional impairment and can be modulated by the local renin–angiotensin system. Full article
(This article belongs to the Special Issue Molecular and CelluIar Mechanisms of Valvular Heart Disease)
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10 pages, 1246 KiB  
Article
Immature Surfactant Protein B Increases in the Serum of Patients with Calcific Severe Aortic Stenosis
by Sonia Eligini, Carlo Savini, Stefania Ghilardi, Alice Mallia, Francesco Vieceli Dalla Sega, Francesca Fortini, Elisa Mikus, Marco Munno, Gloria Modafferi, Piergiuseppe Agostoni, Elena Tremoli and Cristina Banfi
Int. J. Mol. Sci. 2024, 25(12), 6418; https://doi.org/10.3390/ijms25126418 - 11 Jun 2024
Viewed by 1283
Abstract
Valvular disease is a complex pathological condition that impacts countless individuals around the globe. Due to limited treatments, it is crucial to understand its mechanisms to identify new targets. Valve disease may result in pulmonary venous hypertension, which is linked to compromised functioning [...] Read more.
Valvular disease is a complex pathological condition that impacts countless individuals around the globe. Due to limited treatments, it is crucial to understand its mechanisms to identify new targets. Valve disease may result in pulmonary venous hypertension, which is linked to compromised functioning of the alveolar and capillary membranes and hindered gas exchange. Nonetheless, the correlation between surfactant proteins (SPs) and valve disease remains unexplored. A total of 44 patients were enrolled in this study, with 36 undergoing aortic valve replacement and 8 needing a second aortic valve substitution due to bioprosthetic valve degeneration. Ten healthy subjects were also included. The results showed that patients who underwent both the first valve replacement and the second surgery had significantly higher levels of immature SP-B (proSP-B) compared to control subjects. The levels of the extra-lung collectin SP-D were higher in patients who needed a second surgery due to bioprosthetic valve degeneration, while SP-A levels remained unchanged. The research also showed that there was no reciprocal relationship between inflammation and SP-D as the levels of inflammatory mediators did not differ between groups. The present study demonstrates that circulating proSP-B serves as a reliable marker of alveolar–capillary membrane damage in patients with valvular heart disease. Full article
(This article belongs to the Special Issue Molecular and CelluIar Mechanisms of Valvular Heart Disease)
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16 pages, 2310 KiB  
Article
Defining the Role of the miR-145—KLF4—αSMA Axis in Mitral Valvular Interstitial Cell Activation in Myxomatous Mitral Valve Prolapse Using the Canine Model
by Vicky K. Yang, Nicole Moyer, Runzi Zhou, Sally Z. Carnevale, Dawn M. Meola, Sally R. Robinson, Guoping Li and Saumya Das
Int. J. Mol. Sci. 2024, 25(3), 1468; https://doi.org/10.3390/ijms25031468 - 25 Jan 2024
Cited by 1 | Viewed by 1682
Abstract
Mitral valve prolapse (MVP) is a common valvular disease, affecting 2–3% of the adult human population and is a degenerative condition. A total of 5–10% of the afflicted will develop severe mitral regurgitation, cardiac dysfunction, congestive heart failure, and sudden cardiac death. Naturally [...] Read more.
Mitral valve prolapse (MVP) is a common valvular disease, affecting 2–3% of the adult human population and is a degenerative condition. A total of 5–10% of the afflicted will develop severe mitral regurgitation, cardiac dysfunction, congestive heart failure, and sudden cardiac death. Naturally occurring myxomatous MVP in dogs closely resembles MVP in humans structurally, and functional consequences are similar. In both species, valvular interstitial cells (VICs) in affected valves exhibit phenotype consistent with activated myofibroblasts with increased alpha-smooth muscle actin (αSMA) expression. Using VICs collected from normal and MVP-affected valves of dogs, we analyzed the miRNA expression profile of the cells and their associated small extracellular vesicles (sEV) using RNA sequencing to understand the role of non-coding RNAs and sEV in MVP pathogenesis. miR-145 was shown to be upregulated in both the affected VICs and sEV, and overexpression of miR-145 by mimic transfection in quiescent VIC recapitulates the activated myofibroblastic phenotype. Concurrently, KLF4 expression was noted to be suppressed by miR-145, confirming the miR-145—KLF4—αSMA axis. Targeting this axis may serve as a potential therapy in controlling pathologic abnormalities found in MVP valves. Full article
(This article belongs to the Special Issue Molecular and CelluIar Mechanisms of Valvular Heart Disease)
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