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Cardiovascular Diseases Prevention and Therapy

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A special issue of Molecules (ISSN 1420-3049).

Deadline for manuscript submissions: closed (31 March 2019) | Viewed by 44608

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Prof. Dr. Morris Karmazyn

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Retired, Department of Physiology and Pharmacology, University of Western Ontario, London, ON N6G 2X6, Canada
Interests: cardiac hypertrophy; heart failure; sodium hydrogen exchange (NHE1); adipokines; traditional Chinese medicines
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Special Issue Information

Dear Colleagues,

Cardiovascular disease remains a major medical burden throughout most of the world. Despite the underlying complexities involved, development of novel strategies for treating cardiovascular diseases, encompassing abnormalities of the heart and blood vessels, relies strongly on the identification of cellular and molecular mechanisms for treating these disorders. This represents a major challenge for researchers. This Special Issue of Molecules will address the complex fundamental problems underlying cardiovascular disease as they relate to both prevention and treatment. We welcome manuscripts encompassing multifaceted aspects of cardiovascular disease including physiology, pharmacology, and biochemistry with particular emphasis on cellular and molecular phenomena. Both comprehensive experimental studies and review articles will be considered for this Special Issue.

Prof. Dr. Morris Karmazyn
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. Molecules is an international peer-reviewed open access semimonthly 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 2700 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

Cellular and molecular mechanisms of cardiovascular disease
Cardiovascular physiology and pharmacology
New approaches for treatment and prevention of cardiovascular disorders
Dietary approaches for treating cardiovascular disease
In vitro and in vivo models to study cardiovascular disease

Published Papers (6 papers)

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Research

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14 pages, 3430 KiB

Open AccessArticle

Different adaptive NO-dependent Mechanisms in Normal and Hypertensive Conditions

by Michaela Kosutova, Olga Pechanova, Andrej Barta, Sona Franova and Martina Cebova

Molecules 2019, 24(9), 1682; https://doi.org/10.3390/molecules24091682 - 30 Apr 2019

Cited by 8 | Viewed by 2483

Abstract

Myocardial infarction (MI) remains the leading cause of death worldwide. We aimed to investigate the effect of NO deficiency on selective biochemical parameters within discreet myocardial zones after experimentally induced MI. To induce MI, the left descending coronary artery was ligated in two groups of 16-week-old WKY rats. In one group, NO production was inhibited by L-NAME (20 mg/kg/day) administration four weeks prior to ligation. Sham operations were performed on both groups as a control. Seven days after MI, we evaluated levels of nitric oxide synthase (NOS) activity, eNOS, iNOS, NFҡB/p65 and Nrf2 in ischemic, injured and non-ischemic zones of the heart. Levels of circulating TNF-α and IL-6 were evaluated in the plasma. MI led to increased NOS activity in all investigated zones of myocardium as well as circulating levels of TNF-α and IL-6. L-NAME treatment decreased NOS activity in the heart of sham operated animals. eNOS expression was increased in the injured zone and this could be a compensatory mechanism that improves the perfusion of the myocardium and cardiac dysfunction. Conversely, iNOS expression increased in the infarcted zone and may contribute to the inflammatory process and irreversible necrotic changes. Full article

(This article belongs to the Special Issue Cardiovascular Diseases Prevention and Therapy)

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16 pages, 2971 KiB

Open AccessArticle

Cardiac-Specific Cre Induces Age-Dependent Dilated Cardiomyopathy (DCM) in Mice

by Taha Rehmani, Maysoon Salih and Balwant S. Tuana

Molecules 2019, 24(6), 1189; https://doi.org/10.3390/molecules24061189 - 26 Mar 2019

Cited by 13 | Viewed by 5567

Abstract

The genetic modification of the mouse genome using the cre-lox system has been an invaluable tool in deciphering gene and protein function in a temporal and/or spatial manner. However, it has its pitfalls, as researchers have shown that the unregulated expression of cre recombinase can cause DNA damage, the consequences of which can be very detrimental to mouse health. Previously published literature on the most utilized cardiac-specific cre, αMHC-cre, mouse model exhibited a nonlethal hypertrophic cardiomyopathy (HCM) with aging. However, using the same αMHC-cre mice, we observed a cardiac pathology, resulting in complete lethality by 11 months of age. Echocardiography and histology revealed that the αMHC-cre mice were displaying symptoms of dilated cardiomyopathy (DCM) by seven months of age, which ultimately led to their demise in the absence of any HCM at any age. Molecular analysis showed that this phenotype was associated with the DNA damage response through the downregulation of activated p38 and increased expression of JNK, p53, and Bax, known inducers of myocyte death resulting in fibrosis. Our data urges strong caution when interpreting the phenotypic impact of gene responses using αMHC-cre mice, since a lethal DCM was induced by the cre driver in an age-dependent manner in this commonly utilized model system. Full article

(This article belongs to the Special Issue Cardiovascular Diseases Prevention and Therapy)

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17 pages, 3200 KiB

Open AccessArticle

Cardiomyocyte Progenitor Cells as a Functional Gene Delivery Vehicle for Long-Term Biological Pacing

by Anna M. D. Végh, A. Dénise Den Haan, Lucía Cócera Ortega, Arie O. Verkerk, Joost P. G. Sluijter, Diane Bakker, Shirley Van Amersfoorth, Toon A. B. Van Veen, Mischa Klerk, Jurgen Seppen, Jacques M. T. De Bakker, Vincent M. Christoffels, Dirk Geerts, Marie José T. H. Goumans, Hanno L. Tan and Gerard J. J. Boink

Molecules 2019, 24(1), 181; https://doi.org/10.3390/molecules24010181 - 05 Jan 2019

Cited by 9 | Viewed by 4014

Abstract

Sustained pacemaker function is a challenge in biological pacemaker engineering. Human cardiomyocyte progenitor cells (CMPCs) have exhibited extended survival in the heart after transplantation. We studied whether lentivirally transduced CMPCs that express the pacemaker current I_f (encoded by HCN4) can be used as functional gene delivery vehicle in biological pacing. Human CMPCs were isolated from fetal hearts using magnetic beads coated with Sca-1 antibody, cultured in nondifferentiating conditions, and transduced with a green fluorescent protein (GFP)- or HCN4-GFP-expressing lentivirus. A patch-clamp analysis showed a large hyperpolarization-activated, time-dependent inward current (−20 pA/pF at −140 mV, n = 14) with properties typical of I_f in HCN4-GFP-expressing CMPCs. Gap-junctional coupling between CMPCs and neonatal rat ventricular myocytes (NRVMs) was demonstrated by efficient dye transfer and changes in spontaneous beating activity. In organ explant cultures, the number of preparations showing spontaneous beating activity increased from 6.3% in CMPC/GFP-injected preparations to 68.2% in CMPC/HCN4-GFP-injected preparations (P < 0.05). Furthermore, in CMPC/HCN4-GFP-injected preparations, isoproterenol induced a significant reduction in cycle lengths from 648 ± 169 to 392 ± 71 ms (P < 0.05). In sum, CMPCs expressing HCN4-GFP functionally couple to NRVMs and induce physiologically controlled pacemaker activity and may therefore provide an attractive delivery platform for sustained pacemaker function. Full article

(This article belongs to the Special Issue Cardiovascular Diseases Prevention and Therapy)

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Review

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26 pages, 1456 KiB

Open AccessReview

A New Approach for the Prevention and Treatment of Cardiovascular Disorders. Molecular Hydrogen Significantly Reduces the Effects of Oxidative Stress

by Tyler W. LeBaron, Branislav Kura, Barbora Kalocayova, Narcis Tribulova and Jan Slezak

Molecules 2019, 24(11), 2076; https://doi.org/10.3390/molecules24112076 - 31 May 2019

Cited by 99 | Viewed by 21761

Abstract

Cardiovascular diseases are the most common causes of morbidity and mortality worldwide. Redox dysregulation and a dyshomeostasis of inflammation arise from, and result in, cellular aberrations and pathological conditions, which lead to cardiovascular diseases. Despite years of intensive research, there is still no safe and effective method for their prevention and treatment. Recently, molecular hydrogen has been investigated in preclinical and clinical studies on various diseases associated with oxidative and inflammatory stress such as radiation-induced heart disease, ischemia-reperfusion injury, myocardial and brain infarction, storage of the heart, heart transplantation, etc. Hydrogen is primarily administered via inhalation, drinking hydrogen-rich water, or injection of hydrogen-rich saline. It favorably modulates signal transduction and gene expression resulting in suppression of proinflammatory cytokines, excess ROS production, and in the activation of the Nrf2 antioxidant transcription factor. Although H₂ appears to be an important biological molecule with anti-oxidant, anti-inflammatory, and anti-apoptotic effects, the exact mechanisms of action remain elusive. There is no reported clinical toxicity; however, some data suggests that H₂ has a mild hormetic-like effect, which likely mediate some of its benefits. The mechanistic data, coupled with the pre-clinical and clinical studies, suggest that H₂ may be useful for ROS/inflammation-induced cardiotoxicity and other conditions. Full article

(This article belongs to the Special Issue Cardiovascular Diseases Prevention and Therapy)

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15 pages, 2786 KiB

Open AccessReview

Sodium-Hydrogen Exchanger Isoform-1 Inhibition: A Promising Pharmacological Intervention for Resuscitation from Cardiac Arrest

by Raúl J. Gazmuri, Jeejabai Radhakrishnan and Iyad M. Ayoub

Molecules 2019, 24(9), 1765; https://doi.org/10.3390/molecules24091765 - 07 May 2019

Cited by 18 | Viewed by 4168

Abstract

Out-of-hospital sudden cardiac arrest is a major public health problem with an overall survival of less than 5%. Upon cardiac arrest, cessation of coronary blood flow rapidly leads to intense myocardial ischemia and activation of the sarcolemmal Na⁺-H⁺ exchanger isoform-1 (NHE-1). NHE-1 activation drives Na⁺ into cardiomyocytes in exchange for H⁺ with its exchange rate intensified upon reperfusion during the resuscitation effort. Na⁺ accumulates in the cytosol driving Ca²⁺ entry through the Na⁺-Ca²⁺ exchanger, eventually causing cytosolic and mitochondrial Ca²⁺ overload and worsening myocardial injury by compromising mitochondrial bioenergetic function. We have reported clinically relevant myocardial effects elicited by NHE-1 inhibitors given during resuscitation in animal models of ventricular fibrillation (VF). These effects include: (a) preservation of left ventricular distensibility enabling hemodynamically more effective chest compressions, (b) return of cardiac activity with greater electrical stability reducing post-resuscitation episodes of VF, (c) less post-resuscitation myocardial dysfunction, and (d) attenuation of adverse myocardial effects of epinephrine; all contributing to improved survival in animal models. Mechanistically, NHE-1 inhibition reduces adverse effects stemming from Na⁺–driven cytosolic and mitochondrial Ca²⁺ overload. We believe the preclinical work herein discussed provides a persuasive rationale for examining the potential role of NHE-1 inhibitors for cardiac resuscitation in humans. Full article

(This article belongs to the Special Issue Cardiovascular Diseases Prevention and Therapy)

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16 pages, 2553 KiB

Open AccessReview

The Influence of Diet on MicroRNAs that Impact Cardiovascular Disease

by Branislav Kura, Mihir Parikh, Jan Slezak and Grant N. Pierce

Molecules 2019, 24(8), 1509; https://doi.org/10.3390/molecules24081509 - 17 Apr 2019

Cited by 52 | Viewed by 6087

Abstract

Food quality and nutritional habits strongly influence human health status. Extensive research has been conducted to confirm that foods rich in biologically active nutrients have a positive impact on the onset and development of different pathological processes, including cardiovascular diseases. However, the underlying mechanisms by which dietary compounds regulate cardiovascular function have not yet been fully clarified. A growing number of studies confirm that bioactive food components modulate various signaling pathways which are involved in heart physiology and pathology. Recent evidence indicates that microRNAs (miRNAs), small single-stranded RNA chains with a powerful ability to influence protein expression in the whole organism, have a significant role in the regulation of cardiovascular-related pathways. This review summarizes recent studies dealing with the impact of some biologically active nutrients like polyunsaturated fatty acids (PUFAs), vitamins E and D, dietary fiber, or selenium on the expression of many miRNAs, which are connected with cardiovascular diseases. Current research indicates that the expression levels of many cardiovascular-related miRNAs like miRNA-21, -30 family, -34, -155, or -199 can be altered by foods and dietary supplements in various animal and human disease models. Understanding the dietary modulation of miRNAs represents, therefore, an important field for further research. The acquired knowledge may be used in personalized nutritional prevention of cardiovascular disease or the treatment of cardiovascular disorders. Full article

(This article belongs to the Special Issue Cardiovascular Diseases Prevention and Therapy)

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