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Molecular and Cellular Mechanisms in Cardiomyopathy

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 (30 April 2025) | Viewed by 1471

Special Issue Editors


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Guest Editor
Strathclyde Institute of Pharmacy & Biomedical Sciences, University of Strathclyde, Glasgow, UK
Interests: cardiovascular calcium handling in health and disease; in vivo models of cardiac hypertrophy and cardiotoxicity; cardiac fibroblasts; cardiomyocytes; vascular endothelial and smooth muscle cells in health and disease
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Guest Editor
School of Cardiovascular and Metabolic Health, Glasgow Caledonian University, Glasgow, UK
Interests: cardiac calcium handling; cardiac electrophysiology; ryanodine receptors; role of PDEs in CV function; CaMKII

Special Issue Information

Dear Colleagues,

We are pleased to invite contributions to this special issue on Molecular and Cellular Mechanism in Cardiomyopathy. The International Journal of Molecular Sciences is seeking the submission of original articles and review articles covering the scope of altered calcium regulation in cardiovascular disease and potential novel research applications along with therapeutic intervention.

Coordinated regulation of intracellular calcium levels is crucial for healthy cardiovascular function. This is particularly important in cardiac cells given the coupling of calcium cycling to ATP consumption during excitation-contraction coupling. There are a large variety of proteins (exchangers, channels and pumps) that contribute to the tight regulation of calcium transport throughout the cells of the heart. All of these proteins are modulated by a variety of molecular pathways that enable rapid functional changes in response to extracellular chemical or mechanical signals. Under pathological conditions where either acute or chronic cardiovascular stressors are present, there are temporary or sustained alterations in cardiac calcium regulation that can ultimately lead to cardiac hypertrophy, arrhythmias, heart failure and cardiomyopathies. These pathologies result from alterations in molecular signaling that contribute to the dysregulation of calcium handling within the cardiac cell. This special issue will focus on recent advances in our understanding of the defects in cardiac calcium handling which occur during cardiovascular disease. Specific attention will be given to the molecular mechanisms that are responsible for defective cardiovascular function and importantly, possible novel therapeutic interventions that can target these mechanisms and reduce or reverse the pathological phenotype.

We are seeking submissions that may include but are not exclusive to the following topics:

  • Calcium handling in contractile and non-contractile cells of the heart in cardiomyopathy.
  • Alterations in kinase expression, activity and localisation.
  • Role of phosphodiesterases in cardiomyopathy.
  • Alterations in calcium handling proteins in HFpEF versus HFrEF.
  • Novel imaging approaches to assess molecular signaling in cardiomyopathy.
  • Sex differences in calcium handling in cardiomyopathy.
  • Drug therapies to reverse hypertrophy induced alterations in calcium signaling.
  • Arrhythmias as well as class IV antiarrhythmics and calcium channel blockers.

We look forward to receiving your contributions.

Dr. Susan Currie
Dr. Niall MacQuaide
Guest Editors

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

  • E-C coupling
  • cardiac myocyte
  • cardiac fibroblast
  • ryanodine receptor
  • SERCA2a
  • CaMKII
  • phosphodiesterase

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Published Papers (1 paper)

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Review

14 pages, 1020 KiB  
Review
Molecular Mechanisms of L-Type Calcium Channel Dysregulation in Heart Failure
by Arbab Khalid, Abu-Bakr Ahmed, Randeep Gill, Taha Shaikh, Joshua Khorsandi and Ali Kia
Int. J. Mol. Sci. 2025, 26(12), 5738; https://doi.org/10.3390/ijms26125738 - 15 Jun 2025
Viewed by 441
Abstract
The L-type calcium channels (LTCCs) function as the main entry points that convert myocyte membrane depolarization into calcium transients, which drive every heartbeat. There is increasing evidence to show that maladaptive remodeling of these channels is the cause of heart failure with reduced [...] Read more.
The L-type calcium channels (LTCCs) function as the main entry points that convert myocyte membrane depolarization into calcium transients, which drive every heartbeat. There is increasing evidence to show that maladaptive remodeling of these channels is the cause of heart failure with reduced ejection fraction (HFrEF) and heart failure with preserved ejection fraction (HFpEF). Recent experimental, translational, and clinical studies have improved our understanding of the roles LTCC expression, micro-domain trafficking, and post-translational control have in disrupting excitation–contraction coupling, provoking arrhythmias, and shaping phenotype specific hemodynamic compromise. We performed a systematic search of the PubMed and Google Scholar databases (2015–2025, English) and critically evaluated 17 eligible publications in an effort to organize the expanding body of work. This review combines existing data about LTCC density and T-tubule architecture with β-adrenergic and Ca2⁺/calmodulin-dependent protein kinase II (CaMKII) signaling and downstream sarcoplasmic reticulum crosstalk to explain how HFrEF presents with contractile insufficiency and how HFpEF shows diastolic calcium overload and stiffening. Additionally, we highlight the emerging therapeutic strategies aimed at restoring calcium homeostasis such as CaMKII inhibitors, ryanodine receptor type 2 (RyR2) stabilizers, and selective LTCC modulators without compromising systolic reserve. The review establishes LTCC dysregulation as a single mechanism that causes myocardial dysfunction while remaining specific to each phenotype, thus offering clinicians and researchers a complete reference for current concepts and future precision therapy approaches in heart failure. Full article
(This article belongs to the Special Issue Molecular and Cellular Mechanisms in Cardiomyopathy)
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