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IJMS
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Dissecting the Interactions between Cancer, Heart and Anticancer Drug Cardiotoxicity
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Dissecting the Interactions between Cancer, Heart and Anticancer Drug 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 (2 December 2019) | Viewed by 12815

Special Issue Editors

Dr. Carlo Gabriele Tocchetti

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Guest Editor
Department of Translational Medical Sciences, Federico II University, Via Pansini 5, Edificio 2, 80131 Naples, NA, Italy
Interests: cardio-oncology; heart failure
Special Issues, Collections and Topics in MDPI journals
Assist. Prof. Pietro Ameri

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Guest Editor
University of Genova, Italy
Interests: cardio-oncology; heart failure
Dr. Alessandra Ghigo

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Guest Editor
Department of Molecular Biotechnology and Health Sciences, Molecular Biotechnology Center, University of Torino, 10126 Torino, Italy
Interests: cardio-oncology; signaling in cancer and the heart

Special Issue Information

Dear Colleagues,

With the prolongation in life expectancy, a continuously ageing population is more prone to developing chronic diseases. The prevalence of cardiovascular and oncologic disorders is also increasing, and there is an unmet need for life-saving treatments. This Special Issue is calling for original articles and state-of-the-art reviews that address the mechanisms and the clinical scenarios linking cancer, cardiovascular disorders and conventional and novel oncological therapies, in order to update the readers of IJMS with the major advancements in this field. Basic and clinical research are upfront in dissecting the complex, bidirectional interactions between cancer and cardiovascular disorders that frequently lead to an increased risk of cardiotoxicity from antineoplastic drugs, and in the quest for novel therapeutic strategies to fight these problems.

Assoc. Prof. Carlo Gabriele Tocchetti
Assist. Prof. Pietro Ameri
Assist. Prof. Alessandra Ghigo
Guest Editors

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Published Papers (3 papers)

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Research

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13 pages, 2724 KiB  
Article
Cardiac Troponins are Among Targets of Doxorubicin-Induced Cardiotoxicity in hiPCS-CMs
by Michaela Adamcova, Veronika Skarkova, Jitka Seifertova and Emil Rudolf
Int. J. Mol. Sci. 2019, 20(11), 2638; https://doi.org/10.3390/ijms20112638 - 29 May 2019
Cited by 17 | Viewed by 4784
Abstract
Modern diagnostic strategies for early recognition of cancer therapeutics-related cardiac dysfunction involve cardiac troponins measurement. Still, the role of other markers of cardiotoxicity is still unclear. The present study was designed to investigate dynamics of response of human cardiomyocytes derived from induced pluripotent [...] Read more.
Modern diagnostic strategies for early recognition of cancer therapeutics-related cardiac dysfunction involve cardiac troponins measurement. Still, the role of other markers of cardiotoxicity is still unclear. The present study was designed to investigate dynamics of response of human cardiomyocytes derived from induced pluripotent stem cells (hiPCS-CMs) to doxorubicin with the special emphasis on their morphological changes in relation to expression and organization of troponins. The hiPCS-CMs were treated with doxorubicin concentrations (1 and 0.3 µM) for 48 h and followed for next up to 6 days. Exposure of hiPCS-CMs to 1 µM doxorubicininduced suppression of both cardiac troponin T (cTnT) and cardiac troponin I (cTnI) gene expression. Conversely, lower 0.3 µM doxorubicin concentration produced no significant changes in the expression of aforementioned genes. However, the intracellular topography, arrangement, and abundance of cardiac troponin proteins markedly changed after both doxorubicin concentrations. In particular, at 48 h of treatment, both cTnT and cTnI bundles started to reorganize, with some of them forming compacted shapes extending outwards and protruding outside the cells. At later intervals (72 h and onwards), the whole troponin network collapsed and became highly disorganized following, to some degree, overall changes in the cellular shape. Moreover, membrane permeability of cardiomyocytes was increased, and intracellular mitochondrial network rearranged and hypofunctional. Together, our results demonstrate complex effects of clinically relevant doxorubicin concentrations on hiPCS-CM cells including changes in cTnT and cTnI, but also in other cellular compartments contributing to the overall cytotoxicity of this class of cytostatics. Full article
(This article belongs to the Special Issue Dissecting the Interactions between Cancer, Heart and Anticancer Drug Cardiotoxicity)
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16 pages, 7530 KiB  
Article
The BET Bromodomain Inhibitor I-BET-151 Induces Structural and Functional Alterations of the Heart Mitochondria in Healthy Male Mice and Rats
by Jérôme Piquereau, Angèle Boet, Christine Péchoux, Fabrice Antigny, Mélanie Lambert, Mélanie Gressette, Benoît Ranchoux, Natalia Gambaryan, Valérie Domergue, Sharon Mumby, David Montani, Ian M. Adcock, Marc Humbert, Anne Garnier, Catherine Rucker-Martin and Frédéric Perros
Int. J. Mol. Sci. 2019, 20(7), 1527; https://doi.org/10.3390/ijms20071527 - 27 Mar 2019
Cited by 20 | Viewed by 3801
Abstract
The bromodomain and extra-terminal domain family inhibitors (BETi) are a promising new class of anticancer agents. Since numerous anticancer drugs have been correlated to cardiomyopathy, and since BETi can affect non-cancerous tissues, we aimed to investigate in healthy animals any ultrastructural BETi-induced alterations [...] Read more.
The bromodomain and extra-terminal domain family inhibitors (BETi) are a promising new class of anticancer agents. Since numerous anticancer drugs have been correlated to cardiomyopathy, and since BETi can affect non-cancerous tissues, we aimed to investigate in healthy animals any ultrastructural BETi-induced alterations of the heart as compared to skeletal muscle. Male Wistar rats were either treated during 3 weeks with I-BET-151 (2 or 10 mg/kg/day) (W3) or treated for 3 weeks then allowed to recover for another 3 weeks (W6) (3-weeks drug washout). Male C57Bl/6J mice were only treated during 5 days (50 mg/kg/day). We demonstrated the occurrence of ultrastructural alterations and progressive destruction of cardiomyocyte mitochondria after I-BET-151 exposure. Those mitochondrial alterations were cardiac muscle-specific, since the skeletal muscles of exposed animals were similar in ultrastructure presentation to the non-exposed animals. I-BET-151 decreased the respiration rate of heart mitochondria in a dose-dependent manner. At the higher dose, it also decreased mitochondrial mass, as evidenced by reduced right ventricular citrate synthase content. I-BET-151 reduced the right and left ventricular fractional shortening. The concomitant decrease in the velocity-time-integral in both the aorta and the pulmonary artery is also suggestive of an impaired heart function. The possible context-dependent cardiac side effects of these drugs have to be appreciated. Future studies should focus on the basic mechanisms of potential cardiovascular toxicities induced by BETi and strategies to minimize these unexpected complications. Full article
(This article belongs to the Special Issue Dissecting the Interactions between Cancer, Heart and Anticancer Drug Cardiotoxicity)
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Review

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15 pages, 2203 KiB  
Review
Metabolomic Perspectives in Antiblastic Cardiotoxicity and Cardioprotection
by Martino Deidda, Valentina Mercurio, Alessandra Cuomo, Antonio Noto, Giuseppe Mercuro and Christian Cadeddu Dessalvi
Int. J. Mol. Sci. 2019, 20(19), 4928; https://doi.org/10.3390/ijms20194928 - 4 Oct 2019
Cited by 15 | Viewed by 3633
Abstract
Despite advances in supportive and protective therapy for myocardial function, cardiovascular diseases due to antineoplastic therapy—primarily cardiomyopathy associated with contractile dysfunction—remain a major cause of morbidity and mortality. Because of the limitations associated with current therapies, investigators are searching for alternative strategies that [...] Read more.
Despite advances in supportive and protective therapy for myocardial function, cardiovascular diseases due to antineoplastic therapy—primarily cardiomyopathy associated with contractile dysfunction—remain a major cause of morbidity and mortality. Because of the limitations associated with current therapies, investigators are searching for alternative strategies that can timely recognise cardiovascular damage—thus permitting a quick therapeutic approach—or prevent the development of the disease. Damage to the heart can result from both traditional chemotherapeutic agents, such as anthracyclines, and new targeted therapies, such as tyrosine kinase inhibitors. In recent years, metabolomics has proved to be a practical tool to highlight fundamental changes in the metabolic state in several pathological conditions. In this article, we present the state-of-the-art technology with regard to the metabolic mechanisms underlying cardiotoxicity and cardioprotection. Full article
(This article belongs to the Special Issue Dissecting the Interactions between Cancer, Heart and Anticancer Drug Cardiotoxicity)
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