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Advances in Cardiac Disease
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Advances in Cardiac Disease

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: 30 November 2025 | Viewed by 2820

Special Issue Editor

Dr. Daniela Rossin

E-Mail Website
Guest Editor
Department of Clinical and Biological Sciences, University of Turin, 10043 Orbassano, Italy
Interests: cardiac physiopathology; inflammation; oxidative stress; antioxidants

Special Issue Information

Dear Colleagues,

Cardiovascular diseases (CVDs) remain the leading cause of death worldwide, and the global burden of heart disease continues to rise due to population ageing, malnutrition, and sedentary lifestyles. In response, the field of cardiology has experienced a surge in innovative research and technological advancements aimed at improving the prevention, diagnosis, treatment, and management of cardiac conditions. This Special Issue, "Advances in Cardiac Disease", aims to present the latest scientific progress in preventing, diagnosing, and treating cardiovascular diseases, including heart failure, arrhythmias, coronary artery disease, and other acute or chronic conditions. It seeks to explore advanced techniques for studying the molecular mechanisms of cardiac disease pathogenesis, such as regulatory pathways, calcium regulation, metabolism, and mitochondrial function. Special emphasis is placed on fibrosis, oxidative stress, inflammation, and cardiac tissue healing to gain a deeper understanding of the onset and progression of cardiac diseases. This issue encourages collaboration between clinicians, biomedical engineers, and researchers across disciplines, highlighting the importance of personalized and multidisciplinary approaches to bridge the gap between fundamental scientific research and practical applications. We welcome submissions that detail the molecular mechanisms and pathogenesis of cardiac disease. Clinical papers that include biomolecular experiments are also encouraged. Contributions that integrate new insights from a diverse range of disciplines, with the ultimate goal of improving care standards and patient outcomes worldwide, are strongly encouraged.

Dr. Daniela Rossin
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

  • innovative cardiac research
  • multidisciplinary cardiovascular approaches
  • advances in cardio-vascular diagnosis
  • novel cardiac therapies
  • therapeutic strategies

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Further information on MDPI's Special Issue policies can be found here.

Published Papers (2 papers)

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Research

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22 pages, 3652 KiB  
Article
Sodium, Potassium-Adenosine Triphosphatase as a Potential Target of the Anti-Tuberculosis Agents, Clofazimine and Bedaquiline
by Khomotso Mmakola, Marissa Balmith, Helen Steel, Mohamed Said, Moliehi Potjo, Mieke van der Mescht, Nomsa Hlatshwayo, Pieter Meyer, Gregory Tintinger, Ronald Anderson and Moloko Cholo
Int. J. Mol. Sci. 2024, 25(23), 13022; https://doi.org/10.3390/ijms252313022 - 4 Dec 2024
Viewed by 1210
Abstract
Multidrug-resistant tuberculosis (MDR-TB) patients are treated with a standardised, short World Health Organization (WHO) regimen which includes clofazimine (CFZ) and bedaquiline (BDQ) antibiotics. These two antibiotics lead to the development of QT prolongation in patients, inhibiting potassium (K+) uptake by targeting [...] Read more.
Multidrug-resistant tuberculosis (MDR-TB) patients are treated with a standardised, short World Health Organization (WHO) regimen which includes clofazimine (CFZ) and bedaquiline (BDQ) antibiotics. These two antibiotics lead to the development of QT prolongation in patients, inhibiting potassium (K+) uptake by targeting the voltage-gated K+ (Kv)11.1 (hERG) channel of the cardiomyocytes (CMs). However, the involvement of these antibiotics to regulate other K+ transporters of the CMs, as potential mechanisms of QT prolongation, has not been explored. This study determined the effects of CFZ and BDQ on sodium, potassium–adenosine triphosphatase (Na+,K+-ATPase) activity of CMs using rat cardiomyocytes (RCMs). These cells were treated with varying concentrations of CFZ and BDQ individually and in combination (1.25–5 mg/L). Thereafter, Na+,K+-ATPase activity was determined, followed by intracellular adenosine triphosphate (ATP) quantification and cellular viability determination. Furthermore, molecular docking of antibiotics with Na+,K+-ATPase was determined. Both antibiotics demonstrated dose–response inhibition of Na+,K+-ATPase activity of the RCMs. The greatest inhibition was demonstrated by combinations of CFZ and BDQ, followed by BDQ alone and, lastly, CFZ. Neither antibiotic, either individually or in combination, demonstrated cytotoxicity. Molecular docking revealed an interaction of both antibiotics with Na+,K+-ATPase, with BDQ showing higher protein-binding affinity than CFZ. The inhibitory effects of CFZ and BDQ, individually and in combination, on the activity of Na+,K+-ATPase pump of the RCMs highlight the existence of additional mechanisms of QT prolongation by these antibiotics. Full article
(This article belongs to the Special Issue Advances in Cardiac Disease)
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Review

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17 pages, 894 KiB  
Review
Mechanisms and Therapeutic Potential of Multiple Forms of Cell Death in Myocardial Ischemia–Reperfusion Injury
by Shinya Tsurusaki and Eddy Kizana
Int. J. Mol. Sci. 2024, 25(24), 13492; https://doi.org/10.3390/ijms252413492 - 17 Dec 2024
Cited by 1 | Viewed by 1406
Abstract
Programmed cell death, especially programmed necrosis such as necroptosis, ferroptosis, and pyroptosis, has attracted significant attention recently. Traditionally, necrosis was thought to occur accidentally without signaling pathways, but recent discoveries have revealed that molecular pathways regulate certain forms of necrosis, similar to apoptosis. [...] Read more.
Programmed cell death, especially programmed necrosis such as necroptosis, ferroptosis, and pyroptosis, has attracted significant attention recently. Traditionally, necrosis was thought to occur accidentally without signaling pathways, but recent discoveries have revealed that molecular pathways regulate certain forms of necrosis, similar to apoptosis. Accumulating evidence indicates that programmed necrosis is involved in the development of various diseases, including myocardial ischemia–reperfusion injury (MIRI). MIRI occurs when blood flow and oxygen return to an ischemic area, causing excessive production of reactive oxygen species. While this reperfusion is critical for treating myocardial infarction, it inevitably causes cellular damage via oxidative stress. Furthermore, this cellular damage triggers multiple forms of cardiomyocyte death, which is the primary cause of inflammation, cardiac tissue remodeling, and ensuing heart failure. Therefore, understanding the molecular mechanisms of various forms of cell death in MIRI is crucial for therapeutic target discovery. Developing therapeutic strategies to inhibit multiple cell death pathways simultaneously could provide effective protection against MIRI. In this paper, we review the fundamental molecular pathways and MIRI-specific mechanisms of apoptosis, necroptosis, ferroptosis, and pyroptosis. Additionally, we suggest that the simultaneous suppression of multiple cell death pathways could be an effective therapy and identify potential therapeutic targets for implementing this strategy. Full article
(This article belongs to the Special Issue Advances in Cardiac Disease)
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