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Molecular and Cellular Mechanisms Underlying Cardiac Arrhythmias
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Molecular and Cellular Mechanisms Underlying Cardiac Arrhythmias

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

Deadline for manuscript submissions: closed (31 May 2022) | Viewed by 4834

Special Issue Editor

Dr. Peter Michael Kekenes-Huskey

E-Mail Website
Guest Editor
Stritch School of Medicine, Loyola University of Chicago, Chicago, IL, USA
Interests: molecular simulations; systems biology; calcium; reaction-diffusion; cardiac; immune function

Special Issue Information

Dear Colleagues,

We are excited to invite you to contribute your cutting-edge research and perspectives regarding the cellular and molecular mechanisms underlying cardiac arrhythmias. We are seeking contributions that encompass either experimental or theoretical approaches that investigate diverse mechanisms that promote arrhythmias. The intent of this Special Issue is to broaden our understanding of these mechanisms, challenge current dogmas, and prioritize new avenues of research. Mechanisms could include the mutations or alterered expression of cardiac ion channels, post-translational modifications, dysregulated intracellular signaling pathways, and the mismanagement of calcium and sodium. We would be grateful for your contribution to this Special Issue, as well as for any suggestions you may have regarding other researchers whose work aligns with this focus area.

Dr. Peter Michael Kekenes-Huskey
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

  • cardiac
  • channelopathy
  • arrhythmia
  • electrophysiology
  • simulation

Published Papers (2 papers)

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Research

14 pages, 3915 KiB  
Article
Impact of High-Dose Irradiation on Human iPSC-Derived Cardiomyocytes Using Multi-Electrode Arrays: Implications for the Antiarrhythmic Effects of Cardiac Radioablation
by Jae Sik Kim, Seong Woo Choi, Yun-Gwi Park, Sung Joon Kim, Chang Heon Choi, Myung-Jin Cha and Ji Hyun Chang
Int. J. Mol. Sci. 2022, 23(1), 351; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms23010351 - 29 Dec 2021
Cited by 12 | Viewed by 2090
Abstract
Cardiac radioablation is emerging as an alternative option for refractory ventricular arrhythmias. However, the immediate acute effect of high-dose irradiation on human cardiomyocytes remains poorly known. We measured the electrical activities of human induced pluripotent stem cell-derived cardiomyocytes (iPSC-CMs) upon irradiation with 0, [...] Read more.
Cardiac radioablation is emerging as an alternative option for refractory ventricular arrhythmias. However, the immediate acute effect of high-dose irradiation on human cardiomyocytes remains poorly known. We measured the electrical activities of human induced pluripotent stem cell-derived cardiomyocytes (iPSC-CMs) upon irradiation with 0, 20, 25, 30, 40, and 50 Gy using a multi-electrode array, and cardiomyocyte function gene levels were evaluated. iPSC-CMs showed to recover their electrophysiological activities (total active electrode, spike amplitude and slope, and corrected field potential duration) within 3–6 h from the acute effects of high-dose irradiation. The beat rate immediately increased until 3 h after irradiation, but it steadily decreased afterward. Conduction velocity slowed in cells irradiated with ≥25 Gy until 6–12 h and recovered within 24 h; notably, 20 and 25 Gy-treated groups showed subsequent continuous increase. At day 7 post-irradiation, except for cTnT, cardiomyocyte function gene levels increased with increasing irradiation dose, but uniquely peaked at 25–30 Gy. Altogether, high-dose irradiation immediately and reversibly modifies the electrical conduction of cardiomyocytes. Thus, compensatory mechanisms at the cellular level may be activated after the high-dose irradiation acute effects, thereby, contributing to the immediate antiarrhythmic outcome of cardiac radioablation for refractory ventricular arrhythmias. Full article
(This article belongs to the Special Issue Molecular and Cellular Mechanisms Underlying Cardiac Arrhythmias)
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19 pages, 7528 KiB  
Article
H1153Y-KCNH2 Mutation Identified in a Sudden Arrhythmic Death Syndrome Case Alters Channel Gating
by Audrey Farrugia, Kevin Rollet, Jérome Sinniger, Susana Brun, Caroline Spenle, Bertrand Ludes, Omar Taleb and Ayikoe Guy Mensah-Nyagan
Int. J. Mol. Sci. 2021, 22(17), 9235; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22179235 - 26 Aug 2021
Cited by 1 | Viewed by 2196
Abstract
Long QT syndrome is one of the most common hereditary channelopathies inducing fatal arrhythmias and sudden cardiac death. We identified in a sudden arrhythmic death syndrome case a C-term KCNH2 mutation (c.3457C > T; p.His1153Tyr) classified as variant of unknown significance and functional [...] Read more.
Long QT syndrome is one of the most common hereditary channelopathies inducing fatal arrhythmias and sudden cardiac death. We identified in a sudden arrhythmic death syndrome case a C-term KCNH2 mutation (c.3457C > T; p.His1153Tyr) classified as variant of unknown significance and functional impact. Heterologous expression in HEK293 cells combined with western-blot, flow-cytometry, immunocytochemical and microscope analyses shows no modification of channel trafficking to the cell membrane. Electrophysiological studies reveal that the mutation causes a loss of HERG channel function through an alteration of channel biophysical properties that reduces the current density leading to LQT2. These results provide the first functional evidence for H1153Y-KCNH2 mutation-induced abnormal channel properties. They concur with previous biophysical and clinical presentations of a survived patient with another variant that is G1036D. Therefore, the present report importantly highlights the potential severity of variants that may have useful implications for treatment, surveillance, and follow-up of LQT2 patients. Full article
(This article belongs to the Special Issue Molecular and Cellular Mechanisms Underlying Cardiac Arrhythmias)
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