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Heart Diseases: From Molecular Basis to Therapy
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Heart Diseases: From Molecular Basis to Therapy

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 (28 February 2023) | Viewed by 6273

Special Issue Editor

Dr. Hector Barajas-Martinez

E-Mail Website
Guest Editor
Lankenau Institute for Medical Research, 100 Lancaster Ave, Wynnewood, PA 19096, USA
Interests: molecular genetics; sudden cardiac death; ion channels; arrhythmias; translation medicine; pharmacology
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Among the inherited ion channelopathies associated with potentially life-threatening ventricular arrhythmia syndromes in nominally structurally normal hearts are the J-wave syndromes, which include the Brugada (BrS) and early repolarization (ERS) syndromes. These ion channelopathies are responsible for sudden cardiac death (SCD), most often in young adults in the third and fourth decade of life. Although great progress has been made in the past few decades, the genetic basis and molecular mechanisms for such syndromes remains largely unclear.

This Special Issue will focus on basic research on cellular and animal models and patient data and samples, and will collect reviews and original research articles that expand knowledge in the field of J-wave syndromes linked with life-threatening ventricular arrhythmias and sudden cardiac death. Potential topics include, but are not limited to, the contribution of the molecular, ionic, cellular, and genetic mechanisms underlying these primary electrical diseases.

Dr. Hector Barajas-Martinez
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. 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.

Keywords

  • sudden cardiac death
  • Brugada syndrome
  • early repolarization syndrome
  • cardiac arrhythmias
  • ventricular tachycardia
  • ventricular fibrillation
  • inherited cardiac arrhythmia syndromes
  • J-wave syndromes

Published Papers (2 papers)

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Review

24 pages, 998 KiB  
Review
Brugada Syndrome: From Molecular Mechanisms and Genetics to Risk Stratification
by Irene Paula Popa, Dragomir N. Șerban, Minela Aida Mărănducă, Ionela Lăcrămioara Șerban, Bogdan Ionel Tamba and Ionuț Tudorancea
Int. J. Mol. Sci. 2023, 24(4), 3328; https://doi.org/10.3390/ijms24043328 - 7 Feb 2023
Cited by 8 | Viewed by 2954
Abstract
Brugada syndrome (BrS) is a rare hereditary arrhythmia disorder, with a distinctive ECG pattern, correlated with an increased risk of ventricular arrhythmias and sudden cardiac death (SCD) in young adults. BrS is a complex entity in terms of mechanisms, genetics, diagnosis, arrhythmia risk [...] Read more.
Brugada syndrome (BrS) is a rare hereditary arrhythmia disorder, with a distinctive ECG pattern, correlated with an increased risk of ventricular arrhythmias and sudden cardiac death (SCD) in young adults. BrS is a complex entity in terms of mechanisms, genetics, diagnosis, arrhythmia risk stratification, and management. The main electrophysiological mechanism of BrS requires further research, with prevailing theories centered on aberrant repolarization, depolarization, and current-load match. Computational modelling, pre-clinical, and clinical research show that BrS molecular anomalies result in excitation wavelength (k) modifications, which eventually increase the risk of arrhythmia. Although a mutation in the SCN5A (Sodium Voltage-Gated Channel Alpha Subunit 5) gene was first reported almost two decades ago, BrS is still currently regarded as a Mendelian condition inherited in an autosomal dominant manner with incomplete penetrance, despite the recent developments in the field of genetics and the latest hypothesis of additional inheritance pathways proposing a more complex mode of inheritance. In spite of the extensive use of the next-generation sequencing (NGS) technique with high coverage, genetics remains unexplained in a number of clinically confirmed cases. Except for the SCN5A which encodes the cardiac sodium channel NaV1.5, susceptibility genes remain mostly unidentified. The predominance of cardiac transcription factor loci suggests that transcriptional regulation is essential to the Brugada syndrome’s pathogenesis. It appears that BrS is a multifactorial disease, which is influenced by several loci, each of which is affected by the environment. The primary challenge in individuals with a BrS type 1 ECG is to identify those who are at risk for sudden death, researchers propose the use of a multiparametric clinical and instrumental strategy for risk stratification. The aim of this review is to summarize the latest findings addressing the genetic architecture of BrS and to provide novel perspectives into its molecular underpinnings and novel models of risk stratification. Full article
(This article belongs to the Special Issue Heart Diseases: From Molecular Basis to Therapy)
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13 pages, 2522 KiB  
Review
Malondialdehyde as an Important Key Factor of Molecular Mechanisms of Vascular Wall Damage under Heart Diseases Development
by Vadim Z. Lankin, Alla K. Tikhaze and Arthur M. Melkumyants
Int. J. Mol. Sci. 2023, 24(1), 128; https://doi.org/10.3390/ijms24010128 - 21 Dec 2022
Cited by 16 | Viewed by 2699
Abstract
This mini review is devoted to a specific issue: the role of malondialdehyde (MDA)—a secondary product of free radical lipid peroxidation—in the molecular mechanisms of the formation of primary atherosclerotic vascular wall lesions. The principal difference between this review and the available literature [...] Read more.
This mini review is devoted to a specific issue: the role of malondialdehyde (MDA)—a secondary product of free radical lipid peroxidation—in the molecular mechanisms of the formation of primary atherosclerotic vascular wall lesions. The principal difference between this review and the available literature is that it discusses in detail the important role in atherogenesis not of “oxidized” LDL (i.e., LDL particles containing lipohydroperoxides), but of LDL particles chemically modified by the natural low-molecular weight dicarbonyl MDA. To confirm this, we consider the data obtained by us earlier, indicating that “atherogenic” are not LDL oxidized as a result of free radical lipoperoxidation and containing lipohydroperoxy derivatives of phospholipids in the outer layer of particles, but LDL whose apoprotein B-100 has been modified due to the chemical reaction of terminal lysine residue amino groups of the apoB-100 with the aldehyde groups of the MDA (Maillard reaction). In addition, we present our original data proving that MDA injures endothelial glycocalyx that suppress the ability of the endothelium to control arterial tone according to changes in wall shear stress. In summary, this mini review for the first time exhaustively discloses the key role of MDA in atherogenesis. Full article
(This article belongs to the Special Issue Heart Diseases: From Molecular Basis to Therapy)
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