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Biomolecular Mediators in Cardiomyopathies
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Biomolecular Mediators in Cardiomyopathies

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 (30 June 2021) | Viewed by 15748

Special Issue Editors

Prof. Dr. Chih-Yang Huang

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Guest Editor
Cardiovascular and Mitochondrial Related Disease Research Center, Hualien Tzu Chi Hospital, Buddhist Tzu Chi Medical Foundation, Hualien 970, Taiwan
Dr. Marthandam Asokan Shibu

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Guest Editor
Cardiovascular and Mitochondrial Related Disease Research Center, Hualien Tzu Chi Hospital, Buddhist Tzu Chi Medical Foundation, Hualien 970, Taiwan
Dr. Tung-Sheng Chen

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Guest Editor
School of Life Science, National Taiwan Normal University, Taiwan

Special Issue Information

Dear Colleagues,

A report from the American Heart Association (AHA) reveals that about 5.7 million people in the United States have suffered heart failure, and cardiomyopathies are a primary cause for heart failure. The AHA defines cardiomyopathies as “a heterogeneous group of diseases of the myocardium associated with mechanical and/or electric dysfunction that usually (but not invariably) exhibit inappropriate ventricular hypertrophy or dilatation and are due to a variety of causes that frequently are genetic”. Therefore, understanding the multitudinous nature of the genesis and pathological manifestations of cardiomyopathy will help in the prevention and treatment of heart failure.

Cardiomyopathies can be divided into four categories including arrhythmogenic right ventricular cardiomyopathy (ARVC), dilated cardiomyopathy (DCM), hypertrophic cardiomyopathy (HCM), and restrictive cardiomyopathy (RCM). Increasing evidence suggests that several signaling mechanisms are activated in cardiomyopathies, causing apoptosis, inflammation, fibrosis, hypertrophy, or autophagy, and triggering these signals involves activation of certain biomolecular mediators. Although a variety of such mediators have been identified, many remain unknown. This Special Issue encourages original and review articles associated with discovering novel biomolecular mediators in cardiomyopathies. Potential topics include, but are not limited to, the following:

● Novel biomolecular mediators, such as DNA, RNA, or proteins, in cardiomyopathies;
● Omics approaches for discovering biomolecular mediators in cardiomyopathies;
● Novel in vitro/in vivo models for studying cardiomyopathies; and
● Novel signals related to cardiomyopathies.

Prof. Dr. Chih-Yang Huang
Dr. Marthandam Asokan Shibu
Dr. Tung-Sheng Chen
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.

Published Papers (4 papers)

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Research

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15 pages, 4542 KiB  
Article
Cardiac Protective Effect of Kirenol against Doxorubicin-Induced Cardiac Hypertrophy in H9c2 Cells through Nrf2 Signaling via PI3K/AKT Pathways
by Abdullah M. Alzahrani, Peramaiyan Rajendran, Vishnu Priya Veeraraghavan and Hamza Hanieh
Int. J. Mol. Sci. 2021, 22(6), 3269; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22063269 - 23 Mar 2021
Cited by 23 | Viewed by 3538
Abstract
Kirenol (KRL) is a biologically active substance extracted from Herba Siegesbeckiae. This natural type of diterpenoid has been widely adopted for its important anti-inflammatory and anti-rheumatic properties. Despite several studies claiming the benefits of KRL, its cardiac effects have not yet been clarified. [...] Read more.
Kirenol (KRL) is a biologically active substance extracted from Herba Siegesbeckiae. This natural type of diterpenoid has been widely adopted for its important anti-inflammatory and anti-rheumatic properties. Despite several studies claiming the benefits of KRL, its cardiac effects have not yet been clarified. Cardiotoxicity remains a key concern associated with the long-term administration of doxorubicin (DOX). The generation of reactive oxygen species (ROS) causes oxidative stress, significantly contributing to DOX-induced cardiac damage. The purpose of the current study is to investigate the cardio-protective effects of KRL against apoptosis in H9c2 cells induced by DOX. The analysis of cellular apoptosis was performed using the terminal deoxynucleotidyl transferase dUTP nick-end labeling (TUNEL) staining assay and measuring the modulation in the expression levels of proteins involved in apoptosis and Nrf2 signaling, the oxidative stress markers. Furthermore, Western blotting was used to determine cell survival. KRL treatment, with Nrf2 upregulation and activation, accompanied by activation of PI3K/AKT, could prevent the administration of DOX to induce cardiac oxidative stress, remodeling, and other effects. Additionally, the diterpenoid enhanced the activation of Bcl2 and Bcl-xL, while suppressing apoptosis marker proteins. As a result, KRL is considered a potential agent against hypertrophy resulting from cardiac deterioration. The study results show that KRL not only activates the IGF-IR-dependent p-PI3K/p-AKT and Nrf2 signaling pathway, but also suppresses caspase-dependent apoptosis. Full article
(This article belongs to the Special Issue Biomolecular Mediators in Cardiomyopathies)
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18 pages, 2814 KiB  
Article
Cardiac-Specific Overexpression of Catalytically Inactive Corin Reduces Edema, Contractile Dysfunction, and Death in Mice with Dilated Cardiomyopathy
by Ranjana Tripathi, Ryan D. Sullivan, Tai-Hwang M. Fan, Aiilyan K. Houng, Radhika M. Mehta, Guy L. Reed and Inna P. Gladysheva
Int. J. Mol. Sci. 2020, 21(1), 203; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms21010203 - 27 Dec 2019
Cited by 19 | Viewed by 4266
Abstract
Humans with dilated cardiomyopathy (DCM) and heart failure (HF) develop low levels of corin, a multi-domain, cardiac-selective serine protease involved in natriuretic peptide cleavage and sodium and water regulation. However, experimental restoration of corin levels markedly attenuates HF progression. To determine whether the [...] Read more.
Humans with dilated cardiomyopathy (DCM) and heart failure (HF) develop low levels of corin, a multi-domain, cardiac-selective serine protease involved in natriuretic peptide cleavage and sodium and water regulation. However, experimental restoration of corin levels markedly attenuates HF progression. To determine whether the beneficial effects of corin in HF require catalytic activity, we engineered cardiac overexpression of an enzymatically inactive corin transgene (corin-Tg(i)). On a wild-type (WT) background, corin-Tg(i) had no evident phenotypic effects. However, in a well-established genetic model of DCM, corin-Tg(i)/DCM mice had increased survival (p < 0.01 to 0.001) vs. littermate corin-WT/DCM controls. Pleural effusion (p < 0.01), lung edema (p < 0.05), systemic extracellular free water (p < 0.01), and heart weight were decreased (p < 0.01) in corin-Tg(i)/DCM vs. corin-WT/DCM mice. Cardiac ejection fraction and fractional shortening improved (p < 0.01), while ventricular dilation decreased (p < 0.0001) in corin-Tg(i)/DCM mice. Plasma atrial natriuretic peptide, cyclic guanosine monophosphate, and neprilysin were significantly decreased. Cardiac phosphorylated glycogen synthase kinase-3β (pSer9-GSK3β) levels were increased in corin(i)-Tg/DCM mice (p < 0.01). In summary, catalytically inactive corin-Tg(i) decreased fluid retention, improved contractile function, decreased HF biomarkers, and diminished cardiac GSK3β activity. Thus, the protective effects of cardiac corin on HF progression and survival in experimental DCM do not require the serine protease activity of the molecule. Full article
(This article belongs to the Special Issue Biomolecular Mediators in Cardiomyopathies)
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Review

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23 pages, 2008 KiB  
Review
The Emerging Role of Epigenetics in Therapeutic Targeting of Cardiomyopathies
by Christina Pagiatakis and Vittoria Di Mauro
Int. J. Mol. Sci. 2021, 22(16), 8721; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22168721 - 13 Aug 2021
Cited by 14 | Viewed by 2880
Abstract
Cardiomyopathies (CMPs) are a heterogeneous group of myocardial diseases accountable for the majority of cases of heart failure (HF) and/or sudden cardiac death (SCD) worldwide. With the recent advances in genomics, the original classification of CMPs on the basis of morphological and functional [...] Read more.
Cardiomyopathies (CMPs) are a heterogeneous group of myocardial diseases accountable for the majority of cases of heart failure (HF) and/or sudden cardiac death (SCD) worldwide. With the recent advances in genomics, the original classification of CMPs on the basis of morphological and functional criteria (dilated (DCM), hypertrophic (HCM), restrictive (RCM), and arrhythmogenic ventricular cardiomyopathy (AVC)) was further refined into genetic (inherited or familial) and acquired (non-inherited or secondary) forms. Despite substantial progress in the identification of novel CMP-associated genetic variations, as well as improved clinical recognition diagnoses, the functional consequences of these mutations and the exact details of the signaling pathways leading to hypertrophy, dilation, and/or contractile impairment remain elusive. To date, global research has mainly focused on the genetic factors underlying CMP pathogenesis. However, growing evidence shows that alterations in molecular mediators associated with the diagnosis of CMPs are not always correlated with genetic mutations, suggesting that additional mechanisms, such as epigenetics, may play a role in the onset or progression of CMPs. This review summarizes published findings of inherited CMPs with a specific focus on the potential role of epigenetic mechanisms in regulating these cardiac disorders. Full article
(This article belongs to the Special Issue Biomolecular Mediators in Cardiomyopathies)
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14 pages, 1253 KiB  
Review
Molecular Basis of Inflammation in the Pathogenesis of Cardiomyopathies
by Emanuele Monda, Giuseppe Palmiero, Marta Rubino, Federica Verrillo, Federica Amodio, Francesco Di Fraia, Roberta Pacileo, Fabio Fimiani, Augusto Esposito, Annapaola Cirillo, Adelaide Fusco, Elisabetta Moscarella, Giulia Frisso, Maria Giovanna Russo, Giuseppe Pacileo, Paolo Calabrò, Olga Scudiero, Martina Caiazza and Giuseppe Limongelli
Int. J. Mol. Sci. 2020, 21(18), 6462; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms21186462 - 04 Sep 2020
Cited by 37 | Viewed by 4195
Abstract
Cardiomyopathies (CMPs) represent a diverse group of heart muscle diseases, grouped into specific morphological and functional phenotypes. CMPs are associated with mutations in sarcomeric and non-sarcomeric genes, with several suspected epigenetic and environmental mechanisms involved in determining penetrance and expressivity. The understanding of [...] Read more.
Cardiomyopathies (CMPs) represent a diverse group of heart muscle diseases, grouped into specific morphological and functional phenotypes. CMPs are associated with mutations in sarcomeric and non-sarcomeric genes, with several suspected epigenetic and environmental mechanisms involved in determining penetrance and expressivity. The understanding of the underlying molecular mechanisms of myocardial diseases is fundamental to achieving a proper management and treatment of these disorders. Among these, inflammation seems to play an important role in the pathogenesis of CMPs. The aim of the present study is to review the current knowledge on the role of inflammation and the immune system activation in the pathogenesis of CMPs and to identify potential molecular targets for a tailored anti-inflammatory treatment. Full article
(This article belongs to the Special Issue Biomolecular Mediators in Cardiomyopathies)
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