Special Issue "Molecular Basis of Cardiovascular Diseases"

A special issue of Biomolecules (ISSN 2218-273X).

Deadline for manuscript submissions: closed (30 September 2022) | Viewed by 1736

Special Issue Editor

Dr. Glen Pyle
E-Mail Website
Guest Editor
Department of Biomedical Sciences, Ontario Veterinary College, University of Guelph, Guelph, ON, Canada
Interests: molecular basis of heart failure; molecular therapeutics, sex differences in cardiovascular health and disease

Special Issue Information

Dear Colleagues,

Cardiovascular disease is a leading cause of morbidity and mortality globally. Increasing rates of diabetes, the disproportionate growth of hypertension in low- and middle-income countries, coupled with an expanding life expectancy, predict continued worldwide growth of cardiovascular disease for decades to come. The rationale development of effective treatments and diagnostic tools for this emerging epidemic requires an understanding of the molecular basis of cardiovascular disease.

This special issue of Biomolecules seeks original research papers and reviews covering current and emerging topics related to the Molecular Basis of Cardiovascular Diseases. Established areas including ischemia-perfusion injury associated with myocardial infarction and cardiac surgery are encouraged, as are traditionally under-represented topics like sex differences in the pathogenesis of cardiovascular disease. Emerging challenges such as the role of environmental pollutants on cardiovascular health and disease development provide an excellent prospect to expand the scope of cardiovascular medicine, and are welcome for consideration in this special issue. Finally, research that transcends disciplinary boundaries including cardio-oncology and cardio-obstetrics offer the unique opportunity to bring new perspectives to the forefront.

Original research studies and reviews are encouraged to cover the scope of health and disease, from patient to molecule, but with a focus on the molecular basis of disease. We look forward to considering all submissions and working to improve our understanding the Molecular Basis of Cardiovascular Diseases.

Dr. Glen Pyle
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. Biomolecules 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 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.


  • cardiovascular disease
  • cardiology
  • molecular biology
  • heart disease
  • heart failure
  • therapeutics
  • diagnostics
  • hypertension
  • ischemia-reperfusion
  • diabetes

Published Papers (1 paper)

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28 pages, 5247 KiB  
Understanding Calmodulin Variants Affecting Calcium-Dependent Inactivation of L-Type Calcium Channels through Whole-Cell Simulation of the Cardiac Ventricular Myocyte
Biomolecules 2023, 13(1), 72; https://doi.org/10.3390/biom13010072 - 29 Dec 2022
Cited by 1 | Viewed by 1317
Mutations in the calcium-sensing protein calmodulin (CaM) have been linked to two cardiac arrhythmia diseases, Long QT Syndrome 14 (LQT14) and Catecholaminergic Polymorphic Ventricular Tachycardia Type 4 (CPVT4), with varying degrees of severity. Functional characterization of the CaM mutants most strongly [...] Read more.
Mutations in the calcium-sensing protein calmodulin (CaM) have been linked to two cardiac arrhythmia diseases, Long QT Syndrome 14 (LQT14) and Catecholaminergic Polymorphic Ventricular Tachycardia Type 4 (CPVT4), with varying degrees of severity. Functional characterization of the CaM mutants most strongly associated with LQT14 show a clear disruption of the calcium-dependent inactivation (CDI) of the L-Type calcium channel (LCC). CPVT4 mutants on the other hand are associated with changes in their affinity to the ryanodine receptor. In clinical studies, some variants have been associated with both CPVT4 and LQT15. This study uses simulations in a model for excitation–contraction coupling in the rat ventricular myocytes to understand how LQT14 variant might give the functional phenotype similar to CPVT4. Changing the CaM-dependent transition rate by a factor of 0.75 corresponding to the D96V variant and by a factor of 0.90 corresponding to the F142L or N98S variants, in a physiologically based stochastic model of the LCC prolonger, the action potential duration changed by a small amount in a cardiac myocyte but did not disrupt CICR at 1, 2, and 4 Hz. Under beta-adrenergic simulation abnormal excitation–contraction coupling was observed above 2 Hz pacing for the mutant CaM. The same conditions applied under beta-adrenergic stimulation led to the rapid onset of arrhythmia in the mutant CaM simulations. Simulations with the LQT14 mutations under the conditions of rapid pacing with beta-adrenergic stimulation drives the cardiac myocyte toward an arrhythmic state known as Ca2+ overload. These simulations provide a mechanistic link to a disease state for LQT14-associated mutations in CaM to yield a CPVT4 phenotype. The results show that small changes to the CaM-regulated inactivation of LCC promote arrhythmia and underscore the significance of CDI in proper heart function. Full article
(This article belongs to the Special Issue Molecular Basis of Cardiovascular Diseases)
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