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Pharmaceuticals
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Current Frames on Cardiotoxicology of New and Old Anticancer Drugs
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Current Frames on Cardiotoxicology of New and Old Anticancer Drugs

A special issue of Pharmaceuticals (ISSN 1424-8247). This special issue belongs to the section "Pharmacology".

Deadline for manuscript submissions: 8 May 2024 | Viewed by 4175

Special Issue Editor

Prof. Dr. Vera Marisa Costa

E-Mail Website
Guest Editor
UCIBIO, REQUIMTE, Laboratory of Toxicology, Faculty of Pharmacy, University of Porto, Rua de Jorge Viterbo Ferreira, 228, 4050-313 Porto, Portugal
Interests: Cardiotoxicity; cardio-oncology; chemobrain; clinical toxicology
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

The incidence of cancer is growing worldwide, and it is estimated to grow even more in the coming decades. Nonetheless, the life expectancy of cancer patients is improving, due to the combination of old and new therapies and early diagnosis. Still, the cardiotoxicity of anticancer therapies is a leading cause of death and morbidity in cancer patients, making cardio-oncology a focal clinical and scientific field at present. Therefore, a major future challenge in cardiovascular medicine lies in understanding the molecular basis of cardiotoxicity of anticancer therapies, paving the way to the identification of more efficient diagnostic and therapeutic tools or even of genetic determinants of patients’ susceptibility.

It is for this reason that this Special Issue aims to bring together the latest findings in the field of cardio-oncology, involving cell-based studies, preclinical and clinical studies, case reports, and reviews that aim to identify novel mechanisms underlying cardiac remodeling and dysfunction and prompting new pharmacological and non-pharmacological therapeutic solutions.

Prof. Dr. Vera Marisa Costa
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. Pharmaceuticals 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 2900 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.

Keywords

  • cardio-oncology
  • anticancer therapies
  • cardiac dysfunction
  • hypertension
  • heart failure
  • intercellular communication
  • treatment
  • prevention
  • diagnosis
  • cardiac remodelling

Published Papers (3 papers)

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Research

18 pages, 3246 KiB  
Article
The Metabolic Fingerprint of Doxorubicin-Induced Cardiotoxicity in Male CD-1 Mice Fades Away with Time While Autophagy Increases
by Sofia Reis Brandão, Ana Reis-Mendes, Maria João Neuparth, Félix Carvalho, Rita Ferreira and Vera Marisa Costa
Pharmaceuticals 2023, 16(11), 1613; https://doi.org/10.3390/ph16111613 - 15 Nov 2023
Cited by 2 | Viewed by 877
Abstract
The cardiotoxicity of doxorubicin (DOX) may manifest at the beginning/during treatment or years after, compromising patients’ quality of life. We intended to study the cardiac pathways one week (short-term, control 1 [CTRL1] and DOX1 groups) or five months (long-term, CTRL2 and DOX2 groups) [...] Read more.
The cardiotoxicity of doxorubicin (DOX) may manifest at the beginning/during treatment or years after, compromising patients’ quality of life. We intended to study the cardiac pathways one week (short-term, control 1 [CTRL1] and DOX1 groups) or five months (long-term, CTRL2 and DOX2 groups) after DOX administration in adult male CD-1 mice. Control groups were given saline, and DOX groups received a 9.0 mg/Kg cumulative dose. In the short-term, DOX decreased the content of AMP-activated protein kinase (AMPK) while the electron transfer flavoprotein-ubiquinone oxidoreductase (ETF-QO) increased compared to CTRL1, suggesting the upregulation of fatty acids oxidation. Moreover, mitofusin1 (Mfn1) content was decreased in DOX1, highlighting decreased mitochondrial fusion. In addition, increased B-cell lymphoma-2 associated X-protein (BAX) content in DOX1 pointed to the upregulation of apoptosis. Conversely, in the long-term, DOX decreased the citrate synthase (CS) activity and the content of Beclin1 and autophagy protein 5 (ATG5) compared to CTRL2, suggesting decreased mitochondrial density and autophagy. Our study demonstrates that molecular mechanisms elicited by DOX are modulated at different extents over time, supporting the differences on clinic cardiotoxic manifestations with time. Moreover, even five months after DOX administration, meaningful heart molecular changes occurred, reinforcing the need for the continuous cardiac monitoring of patients and determination of earlier biomarkers before clinical cardiotoxicity is set. Full article
(This article belongs to the Special Issue Current Frames on Cardiotoxicology of New and Old Anticancer Drugs)
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14 pages, 2346 KiB  
Article
Hyperhomocysteinaemia Promotes Doxorubicin-Induced Cardiotoxicity in Mice
by Rui Fan, Yao Wang, Jinjin Zhang, Xiangbo An, Shuang Liu, Jie Bai, Jiatian Li, Qiuyue Lin, Yunpeng Xie, Jiawei Liao and Yunlong Xia
Pharmaceuticals 2023, 16(9), 1212; https://doi.org/10.3390/ph16091212 - 28 Aug 2023
Cited by 1 | Viewed by 991
Abstract
Doxorubicin, a widely used chemotherapeutic drug in clinical oncology, causes a series of cardiac side effects referred to as doxorubicin-induced cardiotoxicity. Hyperhomocysteinaemia is an independent risk factor for multiple cardiovascular diseases. However, whether hyperhomocysteinaemia contributes to doxorubicin-induced cardiotoxicity is currently unknown. In this [...] Read more.
Doxorubicin, a widely used chemotherapeutic drug in clinical oncology, causes a series of cardiac side effects referred to as doxorubicin-induced cardiotoxicity. Hyperhomocysteinaemia is an independent risk factor for multiple cardiovascular diseases. However, whether hyperhomocysteinaemia contributes to doxorubicin-induced cardiotoxicity is currently unknown. In this study, we explored the pathogenic effects of hyperhomocysteinaemia induced by dietary methionine supplementation (2% wt/wt in rodent chow) in a mouse model of doxorubicin-induced cardiotoxicity. Our data showed that methionine supplementation doubled serum homocysteine levels, inducing mild hyperhomocysteinaemia. Doxorubicin at a cumulative dosage of 25 mg/kg body weight led to significant weight loss and severe cardiac dysfunction, which were further exacerbated by methionine-induced mild hyperhomocysteinaemia. Doxorubicin-induced cardiac atrophy, cytoplasmic vacuolisation, myofibrillar disarray and loss, as well as cardiac fibrosis, were also exacerbated by methionine-induced mild hyperhomocysteinaemia. Additional folic acid supplementation (0.006% wt/wt) prevented methionine-induced hyperhomocysteinaemia and inhibited hyperhomocysteinaemia-aggravated cardiac dysfunction and cardiomyopathy. In particular, hyperhomocysteinaemia increased both serum and cardiac oxidative stress, which could all be inhibited by folic acid supplementation. Therefore, we demonstrated for the first time that hyperhomocysteinaemia could exacerbate doxorubicin-induced cardiotoxicity in mice, and the pathogenic effects of hyperhomocysteinaemia might at least partially correlate with increased oxidative stress and could be prevented by folic acid supplementation. Our study provides preliminary experimental evidence for the assessment of hyperhomocysteinaemia as a potential risk factor for chemotherapy-induced cardiotoxicity in cancer patients. Full article
(This article belongs to the Special Issue Current Frames on Cardiotoxicology of New and Old Anticancer Drugs)
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16 pages, 2922 KiB  
Article
Pregnenolone Inhibits Doxorubicin-Induced Cardiac Oxidative Stress, Inflammation, and Apoptosis—Role of Matrix Metalloproteinase 2 and NADPH Oxidase 1
by Mohamed A. Morsy, Seham A. Abdel-Gaber, Sahar A. Mokhemer, Mahmoud Kandeel, Wael F. Sedik, Anroop B. Nair, Katharigatta N. Venugopala, Hany Ezzat Khalil, Bandar E. Al-Dhubiab and Mervat Z. Mohamed
Pharmaceuticals 2023, 16(5), 665; https://doi.org/10.3390/ph16050665 - 28 Apr 2023
Cited by 2 | Viewed by 1387
Abstract
The clinical usefulness of doxorubicin (DOX) is limited by its serious adverse effects, such as cardiotoxicity. Pregnenolone demonstrated both anti-inflammatory and antioxidant activity in animal models. The current study aimed to investigate the cardioprotective potential of pregnenolone against DOX-induced cardiotoxicity. After acclimatization, male [...] Read more.
The clinical usefulness of doxorubicin (DOX) is limited by its serious adverse effects, such as cardiotoxicity. Pregnenolone demonstrated both anti-inflammatory and antioxidant activity in animal models. The current study aimed to investigate the cardioprotective potential of pregnenolone against DOX-induced cardiotoxicity. After acclimatization, male Wistar rats were randomly grouped into four groups: control (vehicle-treated), pregnenolone (35 mg/kg/d, p.o.), DOX (15 mg/kg, i.p, once), and pregnenolone + DOX. All treatments continued for seven consecutive days except DOX, which was administered once on day 5. The heart and serum samples were harvested one day after the last treatment for further assays. Pregnenolone ameliorated the DOX-induced increase in markers of cardiotoxicity, namely, histopathological changes and elevated serum levels of creatine kinase-MB and lactate dehydrogenase. Moreover, pregnenolone prevented DOX-induced oxidative changes (significantly lowered cardiac malondialdehyde, total nitrite/nitrate, and NADPH oxidase 1, and elevated reduced glutathione), tissue remodeling (significantly decreased matrix metalloproteinase 2), inflammation (significantly decreased tumor necrosis factor-α and interleukin 6), and proapoptotic changes (significantly lowered cleaved caspase-3). In conclusion, these findings show the cardioprotective effects of pregnenolone in DOX-treated rats. The cardioprotection achieved by pregnenolone treatment can be attributed to its antioxidant, anti-inflammatory, and antiapoptotic actions. Full article
(This article belongs to the Special Issue Current Frames on Cardiotoxicology of New and Old Anticancer Drugs)
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