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Molecular Mechanisms, Pharmacology, Toxicology Involved in Cardiac Function and Dysfunction
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Molecular Mechanisms, Pharmacology, Toxicology Involved in Cardiac Function and Dysfunction

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 (31 August 2020) | Viewed by 12551

Special Issue Editor

Prof. Dr. Joachim Neumann

E-Mail Website
Guest Editor
Director of the Institute of Pharmacology and Toxicology, Faculty of Medicine, Martin-Luther-University Halle-Wittenberg, 06120 Halle (Saale), Germany
Interests: dopamine; histamine; proteinphosphatases; heart failure; arrhythmias; serotonin
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

This Special Issue will deal with original experimental studies on current or new or controversial issues in cardiac functions. More specifically, manuscripts are solicited regarding molecular mechanisms (especially due to gene alterations) of systolic or diastolic heart failure or cardiac hypertrophy. The pharmacology of newer drugs and new aspects in the signal transduction of known drugs are of interest. Moreover, manuscripts describing new untoward, i.e., toxic effects, of drugs used in clinical practice would fall also into the scope of this Special Issue. Furthermore, the putative mechanism(s) of arrhythmias are of interest as far as these arrhythmias are secondary to heart failure and not primary arrhythmias. Another topic that may be addressed is the mechanism(s) of heart failure in aging in humans or relevant aging animal models. Experimental studies and up to date reviews of the underlying mechanisms of heart failure are deemed relevant. Finally, an overview and a critical perspective on drugs tested and being tested currently for heart failure would also be of great interest.

Prof. Dr. Joachim Neumann
Guest Editor

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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.

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Published Papers (3 papers)

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Research

14 pages, 3590 KiB  
Article
Heart Failure Disturbs Gut–Blood Barrier and Increases Plasma Trimethylamine, a Toxic Bacterial Metabolite
by Adrian Drapala, Mateusz Szudzik, Dawid Chabowski, Izabella Mogilnicka, Kinga Jaworska, Katarzyna Kraszewska, Emilia Samborowska and Marcin Ufnal
Int. J. Mol. Sci. 2020, 21(17), 6161; https://doi.org/10.3390/ijms21176161 - 26 Aug 2020
Cited by 25 | Viewed by 3806
Abstract
Trimethylamine (TMA) is a gut bacteria product oxidized by the liver to trimethylamine-N-oxide (TMAO). Clinical evidence suggests that cardiovascular disease is associated with increased plasma TMAO. However, little headway has been made in understanding this relationship on a mechanistic and molecular [...] Read more.
Trimethylamine (TMA) is a gut bacteria product oxidized by the liver to trimethylamine-N-oxide (TMAO). Clinical evidence suggests that cardiovascular disease is associated with increased plasma TMAO. However, little headway has been made in understanding this relationship on a mechanistic and molecular level. We investigated the mechanisms affecting plasma levels of TMAO in Spontaneously Hypertensive Heart Failure (SHHF) rats. Healthy Wistar Kyoto (WKY) and SHHF rats underwent metabolic, hemodynamic, histopathological and biochemical measurements, including tight junction proteins analysis. Stool, plasma and urine samples were evaluated for TMA and TMAO using ultra performance liquid chromatography-mass spectrometry. SHHF presented disturbances of the gut–blood barrier including reduced intestinal blood flow, decreased thickness of the colonic mucosa and alterations in tight junctions, such as claudin 1 and 3, and zonula occludens-1. This was associated with significantly higher plasma levels of TMA and TMAO and increased gut-to-blood penetration of TMA in SHHF compared to WKY. There was no difference in kidney function or liver oxidation of TMA to TMAO between WKY and SHHF. In conclusion, increased plasma TMAO in heart failure rats results from a perturbed gut–blood barrier and increased gut-to-blood passage of TMAO precursor, i.e., TMA. Increased gut-to-blood penetration of bacterial metabolites may be a marker and a mediator of cardiovascular pathology. Full article
(This article belongs to the Special Issue Molecular Mechanisms, Pharmacology, Toxicology Involved in Cardiac Function and Dysfunction)
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16 pages, 2630 KiB  
Article
Circulating miRNAs as Potential Biomarkers Associated with Cardiac Remodeling and Fibrosis in Chagas Disease Cardiomyopathy
by Carolina Kymie Vasques Nonaka, Carolina Thé Macêdo, Bruno Raphael Ribeiro Cavalcante, Adriano Costa de Alcântara, Daniela Nascimento Silva, Milena da Rocha Bezerra, Alex Cleber Improta Caria, Fábio Rocha Fernandes Tavora, João David de Souza Neto, Márcia Maria Noya-Rabelo, Silvia Regina Rogatto, Ricardo Ribeiro dos Santos, Bruno Solano de Freitas Souza and Milena Botelho Pereira Soares
Int. J. Mol. Sci. 2019, 20(16), 4064; https://doi.org/10.3390/ijms20164064 - 20 Aug 2019
Cited by 41 | Viewed by 5195
Abstract
Chagas disease (CD) affects approximately 6–7 million people worldwide, from which 30% develop chronic Chagas cardiomyopathy (CCC), usually after being asymptomatic for years. Currently available diagnostic methods are capable of adequately identifying infected patients, but do not provide information regarding the individual risk [...] Read more.
Chagas disease (CD) affects approximately 6–7 million people worldwide, from which 30% develop chronic Chagas cardiomyopathy (CCC), usually after being asymptomatic for years. Currently available diagnostic methods are capable of adequately identifying infected patients, but do not provide information regarding the individual risk of developing the most severe form of the disease. The identification of biomarkers that predict the progression from asymptomatic or indeterminate form to CCC, may guide early implementation of pharmacological therapy. Here, six circulating microRNAs (miR-19a-3p, miR-21-5p, miR-29b-3p, miR-30a-5p, miR-199b-5p and miR-208a-3p) were evaluated and compared among patients with CCC (n = 28), CD indeterminate form (n = 10) and healthy controls (n = 10). MiR-19a-3p, miR-21-5p, and miR-29b-3p were differentially expressed in CCC patients when compared to indeterminate form, showing a positive correlation with cardiac dysfunction, functional class, and fibrosis, and a negative correlation with ejection fraction and left ventricular strain. Cardiac tissue analysis confirmed increased expression of microRNAs in CCC patients. In vitro studies using human cells indicated the involvement of these microRNAs in the processes of cardiac hypertrophy and fibrosis. Our study suggests that miRNAs are involved in the process of cardiac fibrosis and remodeling presented in CD and indicate a group of miRNAs as potential biomarkers of disease progression in CCC. Full article
(This article belongs to the Special Issue Molecular Mechanisms, Pharmacology, Toxicology Involved in Cardiac Function and Dysfunction)
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12 pages, 1579 KiB  
Article
Electrically-Induced Ventricular Fibrillation Alters Cardiovascular Function and Expression of Apoptotic and Autophagic Proteins in Rat Hearts
by Andras Czegledi, Agnes Tosaki, Alexandra Gyongyosi, Rita Zilinyi, Arpad Tosaki and Istvan Lekli
Int. J. Mol. Sci. 2019, 20(7), 1628; https://doi.org/10.3390/ijms20071628 - 2 Apr 2019
Cited by 8 | Viewed by 2964
Abstract
Background: The pathological heart contractions, called arrhythmias, especially ventricular fibrillation (VF), are a prominent feature of many cardiovascular diseases leading to sudden cardiac death. The present investigation evaluates the effect of electrically stimulated VF on cardiac functions related to autophagy and apoptotic mechanisms [...] Read more.
Background: The pathological heart contractions, called arrhythmias, especially ventricular fibrillation (VF), are a prominent feature of many cardiovascular diseases leading to sudden cardiac death. The present investigation evaluates the effect of electrically stimulated VF on cardiac functions related to autophagy and apoptotic mechanisms in isolated working rat hearts. Methods: Each group of hearts was subjected to 0 (Control), 1, 3, or 10 min of spacing-induced VF, followed by 120 min of recovery period and evaluated for cardiac functions, including aortic flow (AF), coronary flow (CF), cardiac output (CO), stroke volume (SV), and heart rate (HR). Hearts were also evaluated for VF effects on infarcted zone magnitude and Western blot analysis was conducted on heart tissue for expression of the apoptotic biomarker cleaved-caspase-3 and the autophagy proteins: p62, P-mTOR/mTOR, LC3BII/LC3BI ratio, and Atg5-12 complexes. Results: Data revealed that VF induced degradation in AF, CF, CO, and SV, which prominently included-variable post-VF capacity for recovery of normal heart rhythm; increased extent of infarcted heart tissue; altered expression of cleaved-caspase-3 suggesting potential for VF-mediated amplification of apoptosis. VF influence on expression of p62, LC3BII/LC3BI, and Atg5-12 proteins was complex, possibly due to differential effects of VF-induced expression on proteins comprising the autophagic program. Conclusions: VF was observed to cause time-dependent changes in autophagy processes, which with additional analysis under ongoing investigations, likely to yield novel therapeutic targets for the prevention of VF and sudden cardiac death. Full article
(This article belongs to the Special Issue Molecular Mechanisms, Pharmacology, Toxicology Involved in Cardiac Function and Dysfunction)
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