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Cells
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Cardiac Arrhythmias: Molecular, Cellular Mechanism and Biomarkers
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Cardiac Arrhythmias: Molecular, Cellular Mechanism and Biomarkers

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Cells of the Cardiovascular System".

Deadline for manuscript submissions: closed (10 January 2023) | Viewed by 1524

Special Issue Editor

Dr. Coeli M. Lopes

E-Mail Website
Guest Editor
Department of Medicine, Lab Cardiovascular Research Institute (SMD), University of Rochester Medical Center, Rochester, NY, USA
Interests: ion channels; long QT; cell signaling; cardiac arrhythmias
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues, 

Sudden cardiac death, due to cardiac arrhythmia, is a leading cause of death worldwide. Although current knowledge has provided great insight into the molecular basis of cardiac arrhythmias, allowing better prediction of patients at higher risk for arrhythmic events and better treatment, much is still unknown. A cardiac arrhythmia risk can be associated with either inherited mutations or acquired as a result of heart disease and drug treatment, although the combination of genetic and acquired risk is largely unexplored in the field.

The purpose of this Special Issue of Cells is to assemble a collection of articles addressing molecular and cellular mechanisms and biomarkers associated with either increased or decreased risk for cardiac arrhythmias in patients. We especially welcome submissions that relate to novel genetic markers and signaling pathways that will lead to novel risk stratification and treatments for cardiac arrhythmias.

Dr. Coeli Lopes
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. Cells 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

  • KCNQ1
  • KCNH2
  • SCN5A
  • fibrillation
  • atrial
  • ventricular
  • arrhythmogenesis
  • signaling
  • sudden cardiac death

Published Papers (1 paper)

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Research

13 pages, 3792 KiB  
Article
Influence of Age on Hyperoxia-Induced Cardiac Pathophysiology in Type 1 Diabetes Mellitus (T1DM) Mouse Model
by Faizan Saleem, Hussein Mansour, Riddhi Vichare, Yashwant Ayalasomayajula, Jenna Yassine, Anagha Hesaraghatta and Siva Kumar Panguluri
Cells 2023, 12(11), 1457; https://doi.org/10.3390/cells12111457 - 24 May 2023
Cited by 1 | Viewed by 1251
Abstract
Mechanical ventilation often results in hyperoxia, a condition characterized by excess SpO2 levels (>96%). Hyperoxia results in changes in the physiological parameters, severe cardiac remodeling, arrhythmia development, and alteration of cardiac ion channels, all of which can point toward a gradual increase [...] Read more.
Mechanical ventilation often results in hyperoxia, a condition characterized by excess SpO2 levels (>96%). Hyperoxia results in changes in the physiological parameters, severe cardiac remodeling, arrhythmia development, and alteration of cardiac ion channels, all of which can point toward a gradual increase in the risk of developing cardiovascular disease (CVD). This study extends the analysis of our prior work in young Akita mice, which demonstrated that exposure to hyperoxia worsens cardiac outcomes in a type 1 diabetic murine model as compared to wild-type (WT) mice. Age is an independent risk factor, and when present with a major comorbidity, such as type 1 diabetes (T1D), it can further exacerbate cardiac outcomes. Thus, this research subjected aged T1D Akita mice to clinical hyperoxia and analyzed the cardiac outcomes. Overall, aged Akita mice (60 to 68 weeks) had preexisting cardiac challenges compared to young Akita mice. Aged mice were overweight, had an increased cardiac cross-sectional area, and showed prolonged QTc and JT intervals, which are proposed as major risk factors for CVD like intraventricular arrhythmias. Additionally, exposure to hyperoxia resulted in severe cardiac remodeling and a decrease in Kv 4.2 and KChIP2 cardiac potassium channels in these rodents. Based on sex-specific differences, aged male Akita mice had a higher risk of poor cardiac outcomes than aged females. Aged male Akita mice had prolonged RR, QTc, and JT intervals even at baseline normoxic exposure. Moreover, they were not protected against hyperoxic stress through adaptive cardiac hypertrophy, which, at least to some extent, is due to reduced cardiac androgen receptors. This study in aged Akita mice aims to draw attention to the clinically important yet understudied subject of the effect of hyperoxia on cardiac parameters in the presence of preexisting comorbidities. The findings would help revise the provision of care for older T1D patients admitted to ICUs. Full article
(This article belongs to the Special Issue Cardiac Arrhythmias: Molecular, Cellular Mechanism and Biomarkers)
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