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Special Issue "Cardiomyopathy and Vasculopathy: From Molecular Basis to Advanced Therapy"

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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 June 2023) | Viewed by 8080

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Special Issue Editor

Dr. Jonghau Hsu

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Guest Editor

1. Department of Pediatrics, Kaohsiung Medical University Hospital, Kaohsiung 807, Taiwan
2. Department of Pediatrics, School of Medicine, College of Medicine, Kaohsiung Medical University, Kaohsiung 807, Taiwan
3. Graduate Institute of Medicine, College of Medicine, Kaohsiung Medical University, Kaohsiung 807, Taiwan
Interests: vascular biology; congenital heart disease; heart failure; ductus arteriosus

Special Issue Information

Dear Colleagues,

Even with the advances of clinical medicine, cardiovascular disease remains the leading cause of morbidity and mortality in the modern era. Thus, both basic and clinical research for novel mechanisms and therapy of cardiomyopathy and vasculopathy are still needed, to elucidate molecular pathogenesis or therapeutic targets and to reduce mortality and improve the life quality.

To this end, this Special Issue of Biomedicines has as its main objective to gather articles that have a basic research background, a clear translational potential, and clinical applications. Therefore, studies investigating novel molecular mechanisms of cardiovascular diseases, preclinical translational research, and clinical management that can shed some light to this important field are welcome in this Special Issue.

In this Special Issue, we cordially invite researchers as well as clinicians to submit their invaluable studies on cardiovascular disease of children and adults, from bench or bedside. Therefore, original investigations and review articles are welcome.

In conclusion, this Special Issue is to underscore the key importance of both basic and cardiovascular research. Potential topics include but are not limited to the following:

Cardiomyopathy
Congenital heart disease
Biomarkers for cardiovascular disease
Atherosclerosis
Hypertension
Myocardial infarction
Heart failure
Cardiac arrhythmias
Pulmonary vascular disease
Peripheral artery disease
Myocarditis
Pericarditis
Shock

Dr. Jonghau Hsu
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

cardiomyopathy
vascular biology
heart failure
arrhythmia
congenital heart disease
vasoreactivity
remodeling
pathogenesis
myocarditis
pulmonary hypertension

Published Papers (6 papers)

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Research

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Open AccessArticle

Iron Status and Short-Term Recovery after Non-Severe Acute Myocarditis: A Prospective Observational Study

Kamil Aleksander Kobak

and

Biomedicines 2023, 11(8), 2136; https://doi.org/10.3390/biomedicines11082136 - 28 Jul 2023

Viewed by 328

Abstract

Pathomechanisms responsible for recovery from acute myocarditis (MCD) or progression to non-ischemic cardiomyopathy have not been comprehensively investigated. Iron, positioned at the crossroads of inflammation and the energy metabolism of cardiomyocytes, may contribute to the pathophysiology of inflammatory myocardial disease. The aim of this study was to evaluate whether systemic iron parameters are related to myocardial dysfunction in MCD patients. We prospectively enrolled 42 consecutive patients hospitalized for MCD. Their iron status and their clinical, laboratory, and echocardiographic indices were assessed during hospitalization and during ambulatory visits six weeks after discharge. A control group comprising healthy volunteers was recruited. The MCD patients had higher serum ferritin and hepcidin and lower serum iron concentration and transferrin saturation (TSAT) than the healthy controls (all p < 0.01). Six weeks after discharge, the iron status of the MCD patients was already comparable to that of the control group. During hospitalization, lower serum iron and TSAT correlated with higher NT-proBNP (both p < 0.05). In-hospital lower serum iron and TSAT correlated with both a lower left ventricular ejection fraction (LVEF) and worse left ventricular global longitudinal strain at follow-up visits (all p < 0.05). In conclusion, in patients with acute MCD, iron status is altered and normalizes within six weeks. Low serum iron and TSAT are related to greater in-hospital neurohormonal activation and subtle persistent left ventricular dysfunction. Full article

(This article belongs to the Special Issue Cardiomyopathy and Vasculopathy: From Molecular Basis to Advanced Therapy)

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Open AccessArticle

Proteasome Inhibitors Decrease the Viability of Pulmonary Arterial Smooth Muscle Cells by Restoring Mitofusin-2 Expression under Hypoxic Conditions

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Biomedicines 2022, 10(4), 873; https://doi.org/10.3390/biomedicines10040873 - 09 Apr 2022

Cited by 4 | Viewed by 1502

Abstract

Pulmonary hypertension (PH) is a severe progressive disease, and the uncontrolled proliferation of pulmonary artery smooth muscle cells (PASMCs) is one of the main causes. Mitofusin-2 (MFN2) profoundly inhibits cell growth and proliferation in a variety of tumor cell lines and rat vascular smooth muscle cells. Down-regulation of MFN2 is known to contribute to PH. Proteasome inhibitors have been shown to inhibit the proliferation of PASMCs; however, there is no study on the regulation of proteasome inhibitors through MFN-2 in the proliferation of PASMCs, a main pathophysiology of PH. In this study, PASMCs were exposed to hypoxic conditions and the expression of MFN2 and cleaved-PARP1 were detected by Western blotting. The effects of hypoxia and proteasome inhibitors on the cell viability of PASMC cells were detected by CCK8 assay. The results indicated that hypoxia increases the viability and reduces the expression of MFN2 in a PASMCs model. MFN2 overexpression inhibits the hypoxia-induced proliferation of PASMCs. In addition, proteasome inhibitors, bortezomib and marizomib, restored the decreased expression of MFN2 under hypoxic conditions, inhibited hypoxia-induced proliferation and induced the expression of cleaved-PARP1. These results suggest that bortezomib and marizomib have the potential to improve the hypoxia-induced proliferation of PASMCs by restoring MFN2 expression. Full article

(This article belongs to the Special Issue Cardiomyopathy and Vasculopathy: From Molecular Basis to Advanced Therapy)

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Review

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Open AccessReview

Vascular Calcification: In Vitro Models under the Magnifying Glass

Elisa Ceccherini

Antonella Cecchettini

and

Biomedicines 2022, 10(10), 2491; https://doi.org/10.3390/biomedicines10102491 - 06 Oct 2022

Viewed by 1335

Abstract

Vascular calcification is a systemic disease contributing to cardiovascular morbidity and mortality. The pathophysiology of vascular calcification involves calcium salt deposition by vascular smooth muscle cells that exhibit an osteoblast-like phenotype. Multiple conditions drive the phenotypic switch and calcium deposition in the vascular wall; however, the exact molecular mechanisms and the connection between vascular smooth muscle cells and other cell types are not fully elucidated. In this hazy landscape, effective treatment options are lacking. Due to the pathophysiological complexity, several research models are available to evaluate different aspects of the calcification process. This review gives an overview of the in vitro cell models used so far to study the molecular processes underlying vascular calcification. In addition, relevant natural and synthetic compounds that exerted anticalcifying properties in in vitro systems are discussed. Full article

(This article belongs to the Special Issue Cardiomyopathy and Vasculopathy: From Molecular Basis to Advanced Therapy)

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Open AccessReview

The Potential Application and Promising Role of Targeted Therapy in Pulmonary Arterial Hypertension

Meng-Chien Willie Hsieh

and

Biomedicines 2022, 10(6), 1415; https://doi.org/10.3390/biomedicines10061415 - 15 Jun 2022

Cited by 2 | Viewed by 2438

Abstract

Pulmonary arterial hypertension (PAH) is a rare yet serious progressive disorder that is currently incurable. This female-predominant disease unfolds as a pan-vasculopathy that affects all layers of the vessel wall. Five classes of pharmacological agents currently exist to target the three major cellular signaling pathways identified in PAH but are incapable of effectively reversing the disease progression. While several targets have been identified for therapy, none of the current PAH specific therapies are curative and cost-effective as they fail to reverse vascular remodeling and do not address the cancer-like features of PAH. Our purpose is to review the current literature on the therapeutic management of PAH, as well as the molecular targets under consideration for therapy so as to shed light on the potential role and future promise of novel strategies in treating this high-mortality disease. This review study summarizes and discusses the potential therapeutic targets to be employed against PAH. In addition to the three major conventional pathways already used in PAH therapy, targeting PDGF/PDGFR signaling, regulators in glycolytic metabolism, PI3K/AKT pathways, mitochondrial heat shock protein 90 (HSP90), high-mobility group box-1 (HMGB1), and bromodomain and extra-terminal (BET) proteins by using their specific inhibitors, or a pharmacological induction of the p53 expression, could be attractive strategies for treating PAH. Full article

(This article belongs to the Special Issue Cardiomyopathy and Vasculopathy: From Molecular Basis to Advanced Therapy)

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Other

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Open AccessCase Report

A Family with Myh7 Mutation and Different Forms of Cardiomyopathies

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Biomedicines 2023, 11(7), 2065; https://doi.org/10.3390/biomedicines11072065 - 22 Jul 2023

Viewed by 556

Abstract

Background: Hypertrophic cardiomyopathy (HCM) and dilated cardiomyopathy (DCM) are common heart muscle disorders that are caused by pathogenic variants in sarcomere protein genes. In this study, we describe a variant in the MHY7 gene, segregating in a family having three different phenotypes of cardiomyopathies. MYH7 encodes for the myosin heavy-chain β (MHC-β) isoform involved in cardiac muscle contractility. Method and results: We present the case of a family with four members diagnosed with HCM and four members with DCM. The proband is a 42-year-old man diagnosed with HCM. He has an extended family of eight siblings; two of them are diagnosed with HCM and are implantable cardioverter–defibrillator (ICD) carriers. One of the siblings died at the age of 23 after suffering a sudden cardiac arrest and DCM of unknown etiology which was diagnosed at autopsy. Another brother was diagnosed with DCM during a routine echocardiographic exam. Genetic testing was performed for the proband and two of his siblings and a niece of the proband, who suffered a cardiac arrest at the age of nine, all being MYH7 mutation positive. For all four of them, cardiac imaging was performed with different findings. They are ICD carriers as well. Conclusions: Our results reveal three variants in phenotypes of cardiomyopathies in a family with MYH7 mutation associated with high SCD risk and ICD needed for primary and secondary prevention. Full article

(This article belongs to the Special Issue Cardiomyopathy and Vasculopathy: From Molecular Basis to Advanced Therapy)

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Open AccessBrief Report

Cardiac Mesenchymal Stem Cell-like Cells Derived from a Young Patient with Bicuspid Aortic Valve Disease Have a Prematurely Aged Phenotype

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Biomedicines 2022, 10(12), 3143; https://doi.org/10.3390/biomedicines10123143 - 06 Dec 2022

Viewed by 1253

Abstract

There is significant interest in the role of stem cells in cardiac regeneration, and yet little is known about how cardiac disease progression affects native cardiac stem cells in the human heart. In this brief report, cardiac mesenchymal stem cell-like cells (CMSCLC) from the right atria of a 21-year-old female patient with a bicuspid aortic valve and aortic stenosis (referred to as biscuspid aortic valve disease BAVD-CMSCLC), were compared with those of a 78-year-old female patient undergoing coronary artery bypass surgery (referred to as coronary artery disease CAD-CMSCLC). Cells were analyzed for expression of MSC markers, ability to form CFU-Fs, metabolic activity, cell cycle kinetics, expression of NANOG and p16, and telomere length. The cardiac-derived cells expressed MSC markers and were able to form CFU-Fs, with higher rate of formation in CAD-CMSCLCs. BAVD-CMSCLCs did not display normal MSC morphology, had a much lower cell doubling rate, and were less metabolically active than CAD-CMSCLCs. Cell cycle analysis revealed a population of BAVD-CMSCLC in G2/M phase, whereas the bulk of CAD-CMSCLC were in the G0/G1 phase. BAVD-CMSCLC had lower expression of NANOG and shorter telomere lengths, but higher expression of p16 compared with the CAD-CMSCLC. In conclusion, BAVD-CMSCLC have a prematurely aged phenotype compared with CAD-CMSCLC, despite originating from a younger patient. Full article

(This article belongs to the Special Issue Cardiomyopathy and Vasculopathy: From Molecular Basis to Advanced Therapy)

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Special Issue "Cardiomyopathy and Vasculopathy: From Molecular Basis to Advanced Therapy"

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