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Special Issue "Pathogenesis of Cardiac Arrhythmias and Heart Failure"

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

Deadline for manuscript submissions: closed (30 November 2014)

Special Issue Editors

Guest Editor
Prof. Yi-Han Chen (Website)

Key Laboratory of Arrhythmias of the Ministry of Education of China, East Hospital, Tongji University School of Medicine, Shanghai 200120, China
Interests: the mechanisms of cardiac arrhythmias and heart failure
Guest Editor
Prof. Jianmin Cui (Website)

Department of Biomedical Engineering, Washington University, One Brookings Drive, Saint Louis, MO 63130, USA
Interests: molecular basis of bioelectricity and related diseases in nervous and cardiovascular systems; including ion channel function; modulation; ion channel associated diseases; and discovery of drugs that target ion channels

Special Issue Information

Dear colleagues,

Cardiac arrhythmias are any of a group of conditions in which the electrical activity of the heart is irregular or is faster or slower than normal. Up to 50% of patients die suddenly at the first manifestation of cardiac diseases; the majority of these patients die of ventricular fibrillation, a lethal cardiac arrhythmia. Heart failure, a syndrome characterized by inadequate systemic perfusion owing to reduced cardiac pumping, is the most common cause of hospitalization of cardiovascular diseases and imposes a great burden on the healthcare system and society.

Cardiac arrhythmias and heart failure are usually interwoven and react with each other; they have been a prevailing public health problem among humans across all ages. Understanding the pathogenesis of cardiac arrhythmias and heart failure is critical to the development of diagnostic, treatment and preventive strategies. The current understanding of electrophysiological mechanisms of cardiac arrhythmias includes automaticity, triggered activity and reentry, and an understanding of pathogenetic mechanisms of heart failure includes a multitude of biomechanical, hemodynamic, hormonal and pathologic stimuli. However, the molecular pathways of cardiac arrhythmias and heart failure are still elusive, and novel molecular defects and pathways remain to be identified for screening, molecular diagnosis, drug-target development, and personalized medicine.

The special issue seeks the original contribution of work which addresses novel mechanisms of cardiac arrhythmias and heart failure. In particular, major interests will be findings in cellular logistics (endocytosis; exocytosis; molecule trafficking; molecular docking machinery, etc.), organelles (mitochondria, sarcoplasmic reticulum, lysosome and endosome, etc.), ion channels, cell electrophysiology, genetic and epigenetic regulations, molecular and cellular biology, physiology, pathophysiology and pharmacology.

Prof. Yi-Han Chen
Prof. Jianmin Cui
Guest Editors

Submission

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. Papers will be published continuously (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as 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 refereed through a 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 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 1600 CHF (Swiss Francs).

Keywords

  • cardiac arrhythmias
  • heart failure
  • mechanisms
  • physiology and pathophysiology
  • molecular and cellular biology
  • cell and in vivo electrophysiology
  • cellular logistics
  • organelles
  • ion channels
  • genetic and epigenetic regulations

Published Papers (8 papers)

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Research

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Open AccessArticle Serum Selenium and Ceruloplasmin in Nigerians with Peripartum Cardiomyopathy
Int. J. Mol. Sci. 2015, 16(4), 7644-7654; doi:10.3390/ijms16047644
Received: 17 January 2015 / Revised: 7 March 2015 / Accepted: 31 March 2015 / Published: 7 April 2015
Cited by 1 | PDF Full-text (680 KB) | HTML Full-text | XML Full-text
Abstract
The study aimed to determine if selenium deficiency, serum ceruloplasmin and traditional birth practices are risk factors for peripartum cardiomyopathy (PPCM), in Kano, Nigeria. This is a case-control study carried out in three hospitals, and PPCM patients were followed up for six [...] Read more.
The study aimed to determine if selenium deficiency, serum ceruloplasmin and traditional birth practices are risk factors for peripartum cardiomyopathy (PPCM), in Kano, Nigeria. This is a case-control study carried out in three hospitals, and PPCM patients were followed up for six months. Critically low serum selenium concentration was defined as <70 µg/L. A total of 39 PPCM patients and 50 controls were consecutively recruited after satisfying the inclusion criteria. Mean serum selenium in patients (61.7 ± 14.9 µg/L) was significantly lower than in controls (118.4 ± 45.6 µg/L) (p < 0.001). The prevalence of serum selenium <70 µg/L was significantly higher among patients (76.9%) than controls (22.0%) (p < 0.001). The mean ceruloplasmin and prevalence of socio-economic indices, multiparity, pregnancy-induced hypertension, obesity and twin pregnancy were not different between the groups (p > 0.05). Logistic regression showed that rural residency significantly increased the odds for serum selenium <70 µg/L by 2.773-fold (p = 0.037). Baseline serum levels of selenium and ceruloplasmin were not associated with six-month mortality. This study has shown that selenium deficiency is a risk factor for PPCM in Kano, Nigeria, and is related to rural residency. However, serum ceruloplasmin, customary birth practices and some other characteristics were not associated with PPCM in the study area. Full article
(This article belongs to the Special Issue Pathogenesis of Cardiac Arrhythmias and Heart Failure)
Open AccessArticle MiR-25 Protects Cardiomyocytes against Oxidative Damage by Targeting the Mitochondrial Calcium Uniporter
Int. J. Mol. Sci. 2015, 16(3), 5420-5433; doi:10.3390/ijms16035420
Received: 4 January 2015 / Revised: 4 January 2015 / Accepted: 27 February 2015 / Published: 10 March 2015
Cited by 6 | PDF Full-text (3442 KB) | HTML Full-text | XML Full-text
Abstract
MicroRNAs (miRNAs) are a class of small non-coding RNAs, whose expression levels vary in different cell types and tissues. Emerging evidence indicates that tissue-specific and -enriched miRNAs are closely associated with cellular development and stress responses in their tissues. MiR-25 has been [...] Read more.
MicroRNAs (miRNAs) are a class of small non-coding RNAs, whose expression levels vary in different cell types and tissues. Emerging evidence indicates that tissue-specific and -enriched miRNAs are closely associated with cellular development and stress responses in their tissues. MiR-25 has been documented to be abundant in cardiomyocytes, but its function in the heart remains unknown. Here, we report that miR-25 can protect cardiomyocytes against oxidative damage by down-regulating mitochondrial calcium uniporter (MCU). MiR-25 was markedly elevated in response to oxidative stimulation in cardiomyocytes. Further overexpression of miR-25 protected cardiomyocytes against oxidative damage by inactivating the mitochondrial apoptosis pathway. MCU was identified as a potential target of miR-25 by bioinformatical analysis. MCU mRNA level was reversely correlated with miR-25 under the exposure of H2O2, and MCU protein level was largely decreased by miR-25 overexpression. The luciferase reporter assay confirmed that miR-25 bound directly to the 3' untranslated region (UTR) of MCU mRNA. MiR-25 significantly decreased H2O2-induced elevation of mitochondrial Ca2+ concentration, which is likely to be the result of decreased activity of MCU. We conclude that miR-25 targets MCU to protect cardiomyocytes against oxidative damages. This finding provides novel insights into the involvement of miRNAs in oxidative stress in cardiomyocytes. Full article
(This article belongs to the Special Issue Pathogenesis of Cardiac Arrhythmias and Heart Failure)
Open AccessArticle Simvastatin Attenuates the Oxidative Stress, Endothelial Thrombogenicity and the Inducibility of Atrial Fibrillation in a Rat Model of Ischemic Heart Failure
Int. J. Mol. Sci. 2014, 15(8), 14803-14818; doi:10.3390/ijms150814803
Received: 13 May 2014 / Revised: 21 July 2014 / Accepted: 1 August 2014 / Published: 22 August 2014
PDF Full-text (9906 KB) | HTML Full-text | XML Full-text
Abstract
Increased atrial oxidative stress has an important role in inducing and maintaining atrial fibrillation (AF), and the activation of the small GTPase Rac1 contributes to the oxidative stress. We investigated the relationship of Rac1, atrial endothelial thromboprotective markers and AF inducibility and [...] Read more.
Increased atrial oxidative stress has an important role in inducing and maintaining atrial fibrillation (AF), and the activation of the small GTPase Rac1 contributes to the oxidative stress. We investigated the relationship of Rac1, atrial endothelial thromboprotective markers and AF inducibility and if simvastatin has a potential beneficial effect on a myocardial infarction (MI)-induced heart failure (HF) rat model. Rats were randomized into three groups (shams, MI group and simvastatin treatment group) and underwent echocardiography, AF induction studies and left atrial (LA) fibrosis analysis. Atrial Rac 1, sodium calcium exchanger (INCX), sarcoplasmic reticulum calcium ATPase (SERCA), endothelial nitric oxide synthase (eNOS) and induced nitric oxide synthase (iNOS) were measured. AF inducibility, AF duration and LA fibrosis were significantly higher in the MI group (p < 0.001 vs. sham), which were significantly reduced by simvastatin (p < 0.05 vs. MI). The reduced expressions of atrial eNOS, SERCA, thrombomodulin, tissue factor pathway inhibitor and tissue plasminogen activator in the MI group were significantly improved by simvastatin. Furthermore, the increased expression of atrial iNOS, INCX and Rac1 activity were significantly decreased by the simvastatin. Oxidative stress, endothelial dysfunction and thrombogenicity are associated with the promotion of AF in a rat model of ischemic HF. These were associated with increased Rac1 activity, and simvastatin treatment prevents these changes. Full article
(This article belongs to the Special Issue Pathogenesis of Cardiac Arrhythmias and Heart Failure)

Review

Jump to: Research

Open AccessReview Is Correction of Iron Deficiency a New Addition to the Treatment of the Heart Failure?
Int. J. Mol. Sci. 2015, 16(6), 14056-14074; doi:10.3390/ijms160614056
Received: 7 April 2015 / Revised: 5 June 2015 / Accepted: 11 June 2015 / Published: 18 June 2015
Cited by 1 | PDF Full-text (704 KB) | HTML Full-text | XML Full-text
Abstract
Anemia is present in about 40% of heart failure (HF) patients. Iron deficiency (ID) is present in about 60% of the patients with anemia (about 24% of all HF patients) and in about 40% of patients without anemia (about 24% of all [...] Read more.
Anemia is present in about 40% of heart failure (HF) patients. Iron deficiency (ID) is present in about 60% of the patients with anemia (about 24% of all HF patients) and in about 40% of patients without anemia (about 24% of all HF patients). Thus ID is present in about half the patients with HF. The ID in HF is associated with reduced iron stores in the bone marrow and the heart. ID is an independent risk factor for severity and worsening of the HF. Correction of ID with intravenous (IV) iron usually corrects both the anemia and the ID. Currently used IV iron preparations are very safe and effective in treating the ID in HF whereas little information is available on the effectiveness of oral iron. In HF IV iron correction of ID is associated with improvement in functional status, exercise capacity, quality of life and, in some studies, improvement in rate of hospitalization for HF, cardiac structure and function, and renal function. Large long-term adequately-controlled intervention studies are needed to clarify the effect of IV iron in HF. Several heart associations suggest that ID should be routinely sought for in all HF patients and corrected if present. In this paper we present our approach to diagnosis and treatment of iron deficiency in heart failure. Full article
(This article belongs to the Special Issue Pathogenesis of Cardiac Arrhythmias and Heart Failure)
Open AccessReview Potential Role of Dipeptidyl Peptidase IV in the Pathophysiology of Heart Failure
Int. J. Mol. Sci. 2015, 16(2), 4226-4249; doi:10.3390/ijms16024226
Received: 5 January 2014 / Revised: 5 February 2015 / Accepted: 9 February 2015 / Published: 16 February 2015
Cited by 4 | PDF Full-text (1532 KB) | HTML Full-text | XML Full-text
Abstract
Dipeptidyl peptidase IV (DPPIV) is a widely expressed multifunctional serine peptidase that exists as a membrane-anchored cell surface protein or in a soluble form in the plasma and other body fluids. Numerous substrates are cleaved at the penultimate amino acid by DPPIV, [...] Read more.
Dipeptidyl peptidase IV (DPPIV) is a widely expressed multifunctional serine peptidase that exists as a membrane-anchored cell surface protein or in a soluble form in the plasma and other body fluids. Numerous substrates are cleaved at the penultimate amino acid by DPPIV, including glucagon-like peptide-1 (GLP-1), brain natriuretic peptide (BNP) and stromal cell-derived factor-1 (SDF-α), all of which play important roles in the cardiovascular system. In this regard, recent reports have documented that circulating DPPIV activity correlates with poorer cardiovascular outcomes in human and experimental heart failure (HF). Moreover, emerging evidence indicates that DPPIV inhibitors exert cardioprotective and renoprotective actions in a variety of experimental models of cardiac dysfunction. On the other hand, conflicting results have been found when translating these promising findings from preclinical animal models to clinical therapy. In this review, we discuss how DPPIV might be involved in the cardio-renal axis in HF. In addition, the potential role for DPPIV inhibitors in ameliorating heart disease is revised, focusing on the effects of the main DPPIV substrates on cardiac remodeling and renal handling of salt and water. Full article
(This article belongs to the Special Issue Pathogenesis of Cardiac Arrhythmias and Heart Failure)
Open AccessReview Heart Failure and Atrial Fibrillation: From Basic Science to Clinical Practice
Int. J. Mol. Sci. 2015, 16(2), 3133-3147; doi:10.3390/ijms16023133
Received: 29 November 2014 / Accepted: 27 January 2015 / Published: 30 January 2015
Cited by 7 | PDF Full-text (1018 KB) | HTML Full-text | XML Full-text
Abstract
Heart failure (HF) and atrial fibrillation (AF) are two growing epidemics associated with significant morbidity and mortality. They often coexist due to common risk factors and shared pathophysiological mechanisms. Patients presenting with both HF and AF have a worse prognosis and present [...] Read more.
Heart failure (HF) and atrial fibrillation (AF) are two growing epidemics associated with significant morbidity and mortality. They often coexist due to common risk factors and shared pathophysiological mechanisms. Patients presenting with both HF and AF have a worse prognosis and present a particular therapeutic challenge to clinicians. This review aims to appraise the common pathophysiological background, as well as the prognostic and therapeutic implications of coexistent HF and AF. Full article
(This article belongs to the Special Issue Pathogenesis of Cardiac Arrhythmias and Heart Failure)
Open AccessReview Cardiac Arrhythmias and Sleep-Disordered Breathing in Patients with Heart Failure
Int. J. Mol. Sci. 2014, 15(10), 18693-18705; doi:10.3390/ijms151018693
Received: 28 August 2014 / Revised: 28 September 2014 / Accepted: 29 September 2014 / Published: 16 October 2014
Cited by 5 | PDF Full-text (3070 KB) | HTML Full-text | XML Full-text
Abstract
The relationship between heart failure (HF), sleep-disordered breathing and cardiac arrhythmias is complex and poorly understood. Whereas the frequency of predominantly obstructive sleep apnea in HF patients is low and similar or moderately higher to that observed in the general population, central [...] Read more.
The relationship between heart failure (HF), sleep-disordered breathing and cardiac arrhythmias is complex and poorly understood. Whereas the frequency of predominantly obstructive sleep apnea in HF patients is low and similar or moderately higher to that observed in the general population, central sleep apnea (CSA) has been observed in approximately 50% of HF patients, depending on the methods used to detect CSA and patient selection. Despite this high prevalence, it is still unclear whether CSA is merely a marker or an independent risk factor for an adverse prognosis in HF patients and whether CSA is associated with an increased risk for supraventricular as well as ventricular arrhythmias in HF patients. The current review focuses on the relationship between CSA and atrial fibrillation as the most common atrial arrhythmia in HF patients, and on the relationship between CSA and ventricular tachycardia and ventricular fibrillation as the most frequent cause of sudden cardiac death in HF patients. Full article
(This article belongs to the Special Issue Pathogenesis of Cardiac Arrhythmias and Heart Failure)
Open AccessReview The Three Integrated Phases of Left Atrial Macrophysiology and Their Interactions
Int. J. Mol. Sci. 2014, 15(9), 15146-15160; doi:10.3390/ijms150915146
Received: 26 June 2014 / Revised: 17 August 2014 / Accepted: 21 August 2014 / Published: 27 August 2014
Cited by 1 | PDF Full-text (734 KB) | HTML Full-text | XML Full-text
Abstract
Our understanding of the left atrium is growing, although there are many aspects that are still poorly understood. The left atrium size as an imaging biomarker has been consistently shown to be a powerful predictor of outcomes and of different cardiovascular disorders, [...] Read more.
Our understanding of the left atrium is growing, although there are many aspects that are still poorly understood. The left atrium size as an imaging biomarker has been consistently shown to be a powerful predictor of outcomes and of different cardiovascular disorders, such as, but not limited to, atrial fibrillation, congestive heart failure, mitral regurgitation and stroke. Left atrial function has been conventionally divided into three integrated phases: reservoir, conduit and booster-pump. The highly dynamic left atrium and its response to the stretch and secretion of atrial neuropeptides leaves the left atrium far from being a simple transport chamber. The aim of this review is to provide an understanding of the left atrial physiology and its relation to disorders within the heart. Full article
(This article belongs to the Special Issue Pathogenesis of Cardiac Arrhythmias and Heart Failure)
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