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Cellular and Molecular Biology of Heart Diseases 2.0

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A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Biology".

Deadline for manuscript submissions: 30 September 2024 | Viewed by 2435

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Prof. Dr. Kornelia E. Jaquet

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Guest Editor

Department of Cardiology, St. Josef-Hospital and Bergmannsheil, University Clinic of the Ruhr University Bochum, 44801 Bochum, Germany
Interests: molecular mechanism of hereditary cardiomyopathies; protein structure-function relationships; hypertrophic cardiomyopathy; signalling pathways; cell-cell communication via exosomes; post-translational modifications
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Special Issue Information

Dear Colleagues,

Cardiomyopathies are a heterogeneous group of heart muscle diseases with several different phenotypes. They can be classified into inherited and acquired forms, the pathomechanisms of which are the focus of this Special Issue. In cardiomyopathies, either the cardiac muscle cells may be primarily affected or the heart may be the target of various systemic diseases. There is still a large gap in our understanding of the molecular mechanisms of disease development. This missing knowledge is a huge obstacle to the development of specific therapies, especially for the early stage of disease, enabling the inhibition of disease progression.

Inherited and acquired cardiomyopathies are characterized by extensive pathological remodeling of the heart and its cardiomyocytes. Intact structure and intracellular microdomains, the smooth operation of signaling networks, and intercellular communications are essential for the function of cardiomyocytes. Disturbances in these processes and in structural integrity lead to contractile and electrical dysfunction, progressing to heart diseases. In this Special Issue, we intend to cover alterations that may occur in cardiomyopathies. We ask authors to submit papers that provide an improved understanding of Ca²⁺ homoeostasis, protein–protein interactions, post-translational modifications of proteins, the protein quality control system, inflammation processes, mechanosensing, trafficking/communication between cell compartments and between cells, signaling pathways, protein expression and its regulation, and how these factors contribute to the development of disease. As for model systems, we welcome in vitro systems, isolated cardiomyocytes, iPS cells, and tissue or animal models, each having specific limitations and advantages.

Therefore, we especially welcome submissions of original studies that cover one of these topics, but reviews will also be considered.

Dr. Heidi Budde (Heidi.Budde@rub.de), whose central area of research interest is heart disease, is serving as the Co-Guest Editor and will assist Prof. Dr. Kornelia Jaquet in managing this Special Issue.

Prof. Dr. Kornelia E. Jaquet
Guest Editor

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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.

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Keywords

cellular biology
heart disease
cardiomyopathy
pathomechanisms
contractility
signaling
protein interaction
post-translational modification
pathogenic mutation
gene expression

Published Papers (3 papers)

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21 pages, 5476 KiB

Open AccessArticle

Protein Kinase D Plays a Crucial Role in Maintaining Cardiac Homeostasis by Regulating Post-Translational Modifications of Myofilament Proteins

by Melissa Herwig, Merima Begovic, Heidi Budde, Simin Delalat, Saltanat Zhazykbayeva, Marcel Sieme, Luca Schneider, Kornelia Jaquet, Andreas Mügge, Ibrahim Akin, Ibrahim El-Battrawy, Jens Fielitz and Nazha Hamdani

Int. J. Mol. Sci. 2024, 25(5), 2790; https://doi.org/10.3390/ijms25052790 - 28 Feb 2024

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Abstract

Protein kinase D (PKD) enzymes play important roles in regulating myocardial contraction, hypertrophy, and remodeling. One of the proteins phosphorylated by PKD is titin, which is involved in myofilament function. In this study, we aimed to investigate the role of PKD in cardiomyocyte function under conditions of oxidative stress. To do this, we used mice with a cardiomyocyte-specific knock-out of Prkd1, which encodes PKD1 (Prkd1^loxP/loxP; ^αMHC-Cre; PKD1 cKO), as well as wild type littermate controls (Prkd1^loxP/loxP; WT). We isolated permeabilized cardiomyocytes from PKD1 cKO mice and found that they exhibited increased passive stiffness (F_passive), which was associated with increased oxidation of titin, but showed no change in titin ubiquitination. Additionally, the PKD1 cKO mice showed increased myofilament calcium (Ca²⁺) sensitivity (pCa₅₀) and reduced maximum Ca²⁺-activated tension. These changes were accompanied by increased oxidation and reduced phosphorylation of the small myofilament protein cardiac myosin binding protein C (cMyBPC), as well as altered phosphorylation levels at different phosphosites in troponin I (TnI). The increased F_passive and pCa₅₀, and the reduced maximum Ca²⁺-activated tension were reversed when we treated the isolated permeabilized cardiomyocytes with reduced glutathione (GSH). This indicated that myofilament protein oxidation contributes to cardiomyocyte dysfunction. Furthermore, the PKD1 cKO mice exhibited increased oxidative stress and increased expression of pro-inflammatory markers interleukin (IL)-6, IL-18, and tumor necrosis factor alpha (TNF-α). Both oxidative stress and inflammation contributed to an increase in microtubule-associated protein 1 light chain 3 (LC3)-II levels and heat shock response by inhibiting the mammalian target of rapamycin (mTOR) in the PKD1 cKO mouse myocytes. These findings revealed a previously unknown role for PKD1 in regulating diastolic passive properties, myofilament Ca²⁺ sensitivity, and maximum Ca²⁺-activated tension under conditions of oxidative stress. Finally, we emphasized the importance of PKD1 in maintaining the balance of oxidative stress and inflammation in the context of autophagy, as well as cardiomyocyte function. Full article

(This article belongs to the Special Issue Cellular and Molecular Biology of Heart Diseases 2.0)

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16 pages, 8717 KiB

Open AccessArticle

Differences in Mechanical, Electrical and Calcium Transient Performance of the Isolated Right Atrial and Ventricular Myocardium of Guinea Pigs at Different Preloads (Lengths)

by Ruslan Lisin, Alexandr Balakin, Elena Mukhlynina and Yuri Protsenko

Int. J. Mol. Sci. 2023, 24(21), 15524; https://doi.org/10.3390/ijms242115524 - 24 Oct 2023

Viewed by 654

Abstract

There are only a few studies devoted to the comparative and simultaneous study of the mechanisms of the length-dependent regulation of atrial and ventricular contractility. Therefore, an isometric force-length protocol was applied to isolated guinea pig right atrial (RA) strips and ventricular (RV) trabeculae, with a simultaneous measurement of force (Frank–Starling mechanism) and Ca²⁺ transients (CaT) or transmembrane action potentials (AP). Over the entire length-range studied, the duration of isometric contraction, CaT and AP, were shorter in the RA myocardium than in the RV myocardium. The RA myocardium was stiffer than the RV myocardium. With the increasing length of the RA and RV myocardium, the amplitude and duration of isometric contraction and CaT increased, as well as the amplitude and area of the “CaT difference curves” (shown for the first time). However, the rates of the tension development and relaxation decreased. No contribution of AP duration to the heterometric regulation of isometric tension was found in either the RA or RV myocardium of the guinea pig. Changes in the degree of overlap of the contractile proteins of the guinea pig RA and RV myocardium mainly affect CaT kinetics but not AP duration. Full article

(This article belongs to the Special Issue Cellular and Molecular Biology of Heart Diseases 2.0)

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9 pages, 3600 KiB

Open AccessCase Report

The First Korean Case with Cardiac, Facial, and Digital Anomalies with Developmental Delay Caused by De Novo TRAF7 p.Arg655Gln Variant

by Kyung Hee Kim, Ji Yoon Han, Joonhong Park and Jung Sun Cho

Int. J. Mol. Sci. 2024, 25(7), 3701; https://doi.org/10.3390/ijms25073701 - 26 Mar 2024

Viewed by 453

Abstract

TRAF7-related disorders represent some of the rarest inherited disorders, exhibiting clinical features that overlap with cardiac, facial, and digital anomalies with developmental delay (CAFDADD) syndrome, as well as blepharophimosis-mental retardation syndrome (BMRS). A 36-year-old male, presenting with total blindness, blepharophimosis, and intellectual disability, was admitted for the assessment of resting dyspnea several months previously. He had a history of being diagnosed with obstructive sleep apnea (OSA). Transesophageal and transthoracic echocardiography unveiled right ventricular dilatation without significant pulmonary hypertension, bicuspid aortic valve with aortic root aneurysm, and aortic regurgitation in the proband. Sanger sequencing identified a de novo TRAF7 variant (c.1964G>A; p.Arg655Gln). Subsequently, aortic root replacement using the Bentall procedure was performed. However, despite the surgery, he continued to experience dyspnea. Upon re-evaluating OSA with polysomnography, it was discovered that continuous positive airway pressure support alleviated his symptoms. The underlying cause of his symptoms was attributed to OSA, likely exacerbated by the vertebral anomaly and short neck associated with CAFDADD syndrome. Clinicians should be attentive to the symptoms associated with OSA as it is a potentially serious medical condition in patients with TRAF7 variants. Full article

(This article belongs to the Special Issue Cellular and Molecular Biology of Heart Diseases 2.0)

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