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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: 31 May 2024 | Viewed by 912

Special Issue Editors


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Guest Editor
University Hospital Augsburg, Augsburg, Germany
Interests: heart; valvular heart disease; heart valve disorder; myocardial disease

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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

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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

Published Papers (1 paper)

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Research

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
Viewed by 653
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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