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Advances in Molecular Mechanisms of Cardiotoxicity
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Advances in Molecular Mechanisms of Cardiotoxicity

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

Deadline for manuscript submissions: closed (15 September 2023) | Viewed by 10445

Special Issue Editors

Dr. Antonio Lax

E-Mail Website
Guest Editor
Department of Medicine, University of Murcia, 30120 Murcia, Spain
Interests: heart failure; adverse cardiac remodeling; myocardial infarction; cardiotoxicity
Dr. Mari Carmen Asensio-Lopez

E-Mail Website
Guest Editor
Hematovascular Pathophysiology Lab, Spanish National Center for Cardiovascular Research, 28029 Madrid, Spain
Interests: heart failure; adverse remodeling; cardiotoxicity; myocardial infarction; gene therapy

Special Issue Information

Dear Colleagues,

Although the molecular mechanism related to chemotherapy-induced cardiotoxicity is associated with activation of oxidative stress in oncologic patients, studies with a more standardized design and better characterized populations are necessary to evaluate novel molecular axes. Further, the development of new technologies allows the analysis of a large volume of data, which may lead to enabling a more precise description of the molecular processes related to cardiotoxicity after chemotherapy.

Here, I propose an ambitious program to change the conceptual framework used for the management of cardio-oncological issues. The aim will be to detail novel molecular mechanisms related to cardiotoxicity, with novel pharmacological targets described to design pioneering therapies to treat or prevent cardiotoxicity related to chemotherapeutic treatments.

Dr. Antonio Lax
Dr. Mari Carmen Asensio-Lopez
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

  • cardiac dysfunction
  • cardiotoxicity
  • atrophy
  • antagomiR
  • AAV
  • gene therapy
  • heart failure
  • oxidative stress
  • apoptosis
  • myocardial remodeling

Published Papers (5 papers)

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Research

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15 pages, 7515 KiB  
Article
Unraveling Structural Alerts in Marketed Drugs for Improving Adverse Outcome Pathway Framework of Drug-Induced QT Prolongation
by Wulin Long, Shihai Li, Yujie He, Jinzhu Lin, Menglong Li and Zhining Wen
Int. J. Mol. Sci. 2023, 24(7), 6771; https://doi.org/10.3390/ijms24076771 - 05 Apr 2023
Viewed by 1498
Abstract
In pharmaceutical treatment, many non-cardiac drugs carry the risk of prolonging the QT interval, which can lead to fatal cardiac complications such as torsades de points (TdP). Although the unexpected blockade of ion channels has been widely considered to be one of the [...] Read more.
In pharmaceutical treatment, many non-cardiac drugs carry the risk of prolonging the QT interval, which can lead to fatal cardiac complications such as torsades de points (TdP). Although the unexpected blockade of ion channels has been widely considered to be one of the main reasons for affecting the repolarization phase of the cardiac action potential and leading to QT interval prolongation, the lack of knowledge regarding chemical structures in drugs that may induce the prolongation of the QT interval remains a barrier to further understanding the underlying mechanism and developing an effective prediction strategy. In this study, we thoroughly investigated the differences in chemical structures between QT-prolonging drugs and drugs with no drug-induced QT prolongation (DIQT) concerns, based on the Drug-Induced QT Prolongation Atlas (DIQTA) dataset. Three categories of structural alerts (SAs), namely amines, ethers, and aromatic compounds, appeared in large quantities in QT-prolonging drugs, but rarely in drugs with no DIQT concerns, indicating a close association between SAs and the risk of DIQT. Moreover, using the molecular descriptors associated with these three categories of SAs as features, the structure–activity relationship (SAR) model for predicting the high risk of inducing QT interval prolongation of marketed drugs achieved recall rates of 72.5% and 80.0% for the DIQTA dataset and the FDA Adverse Event Reporting System (FAERS) dataset, respectively. Our findings may promote a better understanding of the mechanism of DIQT and facilitate research on cardiac adverse drug reactions in drug development. Full article
(This article belongs to the Special Issue Advances in Molecular Mechanisms of Cardiotoxicity)
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15 pages, 1765 KiB  
Article
Increased Intracellular Free Zinc Has Pleiotropic Effects on Doxorubicin-Induced Cytotoxicity in hiPCS-CMs Cells
by Kamil Rudolf and Emil Rudolf
Int. J. Mol. Sci. 2023, 24(5), 4518; https://doi.org/10.3390/ijms24054518 - 24 Feb 2023
Viewed by 1088
Abstract
(1) the mechanisms and outcomes of doxorubicin (DOX)-dependent toxicity upon changed intracellular zinc (Zn) concentrations in the cardiomyocytes obtained from human-induced pluripotent stem cells (hiPCS-CMs) were investigated; (2) cells exposed to the DOX were pretreated or cotreated with zinc pyrythione (ZnPyr) and various [...] Read more.
(1) the mechanisms and outcomes of doxorubicin (DOX)-dependent toxicity upon changed intracellular zinc (Zn) concentrations in the cardiomyocytes obtained from human-induced pluripotent stem cells (hiPCS-CMs) were investigated; (2) cells exposed to the DOX were pretreated or cotreated with zinc pyrythione (ZnPyr) and various cellular endpoints and mechanisms were analyzed via cytometric methods; (3) both DOX concentrations (0.3 and 1 µM) induced a concentration-dependent loss of viability, an activation of autophagy, cell death, and the appearance of senescence. These phenotypes were preceded by an oxidative burst, DNA damage, and a loss of mitochondrial and lysosomal integrity. Furthermore, in DOX-treated cells, proinflammatory and stress kinase signaling (in particular, JNK and ERK) were upregulated upon the loss of free intracellular Zn pools. Increased free Zn concentrations proved to have both inhibitory and stimulatory effects on the investigated DOX-related molecular mechanisms, as well as on signaling pathways on the resulting cell fates; and (4) free intracellular Zn pools, their status, and their elevation might have, in a specific context, a pleiotropic impact upon DOX-dependent cardiotoxicity. Full article
(This article belongs to the Special Issue Advances in Molecular Mechanisms of Cardiotoxicity)
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Review

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27 pages, 1441 KiB  
Review
Mitigation of Cardiovascular Disease and Toxicity through NRF2 Signalling
by James A. Roberts, Richard D. Rainbow and Parveen Sharma
Int. J. Mol. Sci. 2023, 24(7), 6723; https://doi.org/10.3390/ijms24076723 - 04 Apr 2023
Cited by 3 | Viewed by 2020
Abstract
Cardiovascular toxicity and diseases are phenomena that have a vastly detrimental impact on morbidity and mortality. The pathophysiology driving the development of these conditions is multifactorial but commonly includes the perturbance of reactive oxygen species (ROS) signalling, iron homeostasis and mitochondrial bioenergetics. The [...] Read more.
Cardiovascular toxicity and diseases are phenomena that have a vastly detrimental impact on morbidity and mortality. The pathophysiology driving the development of these conditions is multifactorial but commonly includes the perturbance of reactive oxygen species (ROS) signalling, iron homeostasis and mitochondrial bioenergetics. The transcription factor nuclear factor erythroid 2 (NFE2)-related factor 2 (NRF2), a master regulator of cytoprotective responses, drives the expression of genes that provide resistance to oxidative, electrophilic and xenobiotic stresses. Recent research has suggested that stimulation of the NRF2 signalling pathway can alleviate cardiotoxicity and hallmarks of cardiovascular disease progression. However, dysregulation of NRF2 dynamic responses can be severely impacted by ageing processes and off-target toxicity from clinical medicines including anthracycline chemotherapeutics, rendering cells of the cardiovascular system susceptible to toxicity and subsequent tissue dysfunction. This review addresses the current understanding of NRF2 mechanisms under homeostatic and cardiovascular pathophysiological conditions within the context of wider implications for this diverse transcription factor. Full article
(This article belongs to the Special Issue Advances in Molecular Mechanisms of Cardiotoxicity)
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14 pages, 1028 KiB  
Review
Radiation Treatment Mechanisms of Cardiotoxicity: A Systematic Review
by Konstantinos C. Siaravas, Christos S. Katsouras and Chrissa Sioka
Int. J. Mol. Sci. 2023, 24(7), 6272; https://doi.org/10.3390/ijms24076272 - 27 Mar 2023
Cited by 2 | Viewed by 1820
Abstract
Radiotherapy may be used alone or in combination with chemotherapy for cancer treatment. There are many mechanisms of radiation treatment exposure to toxicities. Our aim was to summarize the literature about known mechanisms of radiation-induced cardiac toxicities. We performed a systematic review of [...] Read more.
Radiotherapy may be used alone or in combination with chemotherapy for cancer treatment. There are many mechanisms of radiation treatment exposure to toxicities. Our aim was to summarize the literature about known mechanisms of radiation-induced cardiac toxicities. We performed a systematic review of the literature on the PubMed database until October 2022 about cardiovascular toxicities and radiation therapy exposure. Only systematic reviews, meta-analyses, and reviews were selected. Out of 1429 publications screened, 43 papers met inclusion criteria and were selected for the umbrella review process. Microvascular and macrovascular complications could lead to adverse cardiac effects. Many radiotherapy-associated risk factors were responsible, such as the site of radiation treatment, beam proximity to heart tissues, total dosage, the number of radiotherapy sessions, adjuvant chemotherapeutic agents used, and patient traditional cardiovascular risk factors, patient age, and gender. Moreover, important dosage cutoff values could increase the incidence of cardiac toxicities. Finally, the time from radiation exposure to cardiac side effects was assessed. Our report highlighted mechanisms, radiation dosage values, and the timeline of cardiovascular toxicities after radiation therapy. All of the above may be used for the assessment of cardiovascular risk factors and the development of screening programs for cancer patients. Full article
(This article belongs to the Special Issue Advances in Molecular Mechanisms of Cardiotoxicity)
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22 pages, 1679 KiB  
Review
The Innate Immune System in Cardiovascular Diseases and Its Role in Doxorubicin-Induced Cardiotoxicity
by Anchit Bhagat, Pradeep Shrestha and Eugenie S. Kleinerman
Int. J. Mol. Sci. 2022, 23(23), 14649; https://doi.org/10.3390/ijms232314649 - 24 Nov 2022
Cited by 15 | Viewed by 3188
Abstract
Innate immune cells are the early responders to infection and tissue damage. They play a critical role in the initiation and resolution of inflammation in response to insult as well as tissue repair. Following ischemic or non-ischemic cardiac injury, a strong inflammatory response [...] Read more.
Innate immune cells are the early responders to infection and tissue damage. They play a critical role in the initiation and resolution of inflammation in response to insult as well as tissue repair. Following ischemic or non-ischemic cardiac injury, a strong inflammatory response plays a critical role in the removal of cell debris and tissue remodeling. However, persistent inflammation could be detrimental to the heart. Studies suggest that cardiac inflammation and tissue repair needs to be tightly regulated such that the timely resolution of the inflammation may prevent adverse cardiac damage. This involves the recognition of damage; activation and release of soluble mediators such as cytokines, chemokines, and proteases; and immune cells such as monocytes, macrophages, and neutrophils. This is important in the context of doxorubicin-induced cardiotoxicity as well. Doxorubicin (Dox) is an effective chemotherapy against multiple cancers but at the cost of cardiotoxicity. The innate immune system has emerged as a contributor to exacerbate the disease. In this review, we discuss the current understanding of the role of innate immunity in the pathogenesis of cardiovascular disease and dox-induced cardiotoxicity and provide potential therapeutic targets to alleviate the damage. Full article
(This article belongs to the Special Issue Advances in Molecular Mechanisms of Cardiotoxicity)
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