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Cardiovascular Protection against Chemotherapeutics and Environmental Toxins: New Agents and Molecular Targets

A special issue of Molecules (ISSN 1420-3049). This special issue belongs to the section "Medicinal Chemistry".

Deadline for manuscript submissions: closed (31 May 2022) | Viewed by 6727

Special Issue Editors


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Guest Editor
BIDMC Cardiology, Harvard Medical School, Boston, MA, USA
Interests: cardiovascular pharmacology; cardio-Oncology; molecular medicine
Special Issues, Collections and Topics in MDPI journals

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Guest Editor
Great Plains Health, Callahan Cancer Center, North Platte, NE, USA
Interests: cardiology; cardio-oncology; cardiac imaging
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Guest Editor
Cleveland Clinic Foundation, Cleveland, OH, USA
Interests: ischemia/reperfusion injury; myocardial infarction; cardiomyopathy
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Guest Editor
1. Chemistry Department, Faculty of Science, Suez Canal University, Ismailia 41522, Egypt
2. Institute for Chemistry, Humboldt Universität zu Berlin, Brook-Taylor-Str. 2, 12489 Berlin, Germany
Interests: synthetic organic chemistry; synthetic medicinal chemistry; stereochemistry; Heterocyclic Chemistry; drug synthesis and development; small molecule drug discovery by high-throughput library screening; computer aided drug design (modelling, virtual screening); chemistry of lipids; role of lipids in human diseases; development of biochemical tools to study structure and function of lipids; development of enzymatic assays
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Guest Editor
1. Department of Pharmaceutical Sciences, Pharmacy Program, Batterjee Medical College, P.O. Box 6231, Jeddah 21442, Saudi Arabia
2. Pharmacology Department, Faculty of Veterinary Medicine, Suez Canal University, Ismailia, Egypt
Interests: pharmacology; drug toxicology; alternative medicine; environmental pharmacology and toxicology
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

The characterization, management, and prevention of cardiotoxicity, whether caused by pharmacological agents (cardiovascular and non-cardiovascular) or environmental exposures, compose a growing area of research. Cancer chemotherapeutics, in particular, have multiple off-target effects on the cardiovascular system, and studying these effects has led to the birth of the new cardio-oncology field. This Special Issue aims to present the latest advances in the study of cardiotoxicity and especially the field of cardio-oncology, in order to better understand the underlying mechanisms and improve the cardiac safety of therapeutic interventions. Potential topics include, but are not limited to:

  • Cardiac effects, molecular mechanisms, and signaling pathways of drugs, xenobiotics, and environmental toxins
  • Cardiovascular effects of classic cancer chemotherapeutics (e.g., anthracyclines) and new agents (e.g., immune checkpoint inhibitors)
  • Safety and efficacy of novel cardioprotective agents against cardiotoxicity
  • Development and validation of in vivo and in vitro models to study cardiotoxicity

You may choose our Joint Special Issue in Diseases.

Dr. Abdelrahman I. Abushouk
Dr. Kartik Anand
Dr. Anas Saad
Dr. Essa M. Saied
Dr. Mohamed M. Abdel-Daim
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. Molecules is an international peer-reviewed open access semimonthly 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 2700 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

  • cardiotoxicity
  • cardioprotection
  • cardio-oncology
  • cardiovascular pharmacology
  • molecular cardiology

Published Papers (2 papers)

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Research

14 pages, 2631 KiB  
Article
Myocardial Injury Caused by Chronic Alcohol Exposure—A Pilot Study Based on Proteomics
by Xiaonan Ma, Zihan Liao, Rongxuan Li, Wei Xia, Honghui Guo, Jiawei Luo, Huaxin Sheng, Meihui Tian and Zhipeng Cao
Molecules 2022, 27(13), 4284; https://doi.org/10.3390/molecules27134284 - 03 Jul 2022
Cited by 3 | Viewed by 1892
Abstract
Chronic alcohol exposure can cause myocardial degenerative diseases, manifested as cardiac insufficiency, arrhythmia, etc. These are defined as alcoholic cardiomyopathy (ACM). Alcohol-mediated myocardial injury has previously been studied through metabolomics, and it has been proved to be involved in the Kyoto Encyclopedia of [...] Read more.
Chronic alcohol exposure can cause myocardial degenerative diseases, manifested as cardiac insufficiency, arrhythmia, etc. These are defined as alcoholic cardiomyopathy (ACM). Alcohol-mediated myocardial injury has previously been studied through metabolomics, and it has been proved to be involved in the Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway concerning unsaturated fatty acids biosynthesis and oxidative phosphorylation, which tentatively explored the mechanism of ACM induced by chronic drinking. To further study alcohol-induced myocardial injury, myocardial specimens from a previously successfully established mouse model of ACM were subjected to histological, echocardiographic, and proteomic analyses, and validated by real-time quantitative polymerase chain reaction (qPCR). Results of histopathology and echocardiography showed the hypertrophy of cardiomyocytes, the dilation of ventricles, and decreased cardiac function. Proteomic results, available via ProteomeXchange with identifier PXD032949, revealed 56 differentially expressed proteins (DEPs) were identified, which have the potential to be involved in the KEGG pathway related to fatty acid biosynthesis disorders, lipid metabolism disorders, oxidative stress, and, ultimately, in the development of dilated cardiomyopathy (DCM). The present study further elucidates the underlying effects of myocardial injury due to chronic alcohol intake, laying a foundation for further studies to clarify the potential mechanisms of ACM. Full article
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14 pages, 3230 KiB  
Article
Cryptotanshinone Ameliorates Doxorubicin-Induced Cardiotoxicity by Targeting Akt-GSK-3β-mPTP Pathway In Vitro
by Xiaoping Wang, Qianbin Sun, Qianqian Jiang, Yanyan Jiang, Yawen Zhang, Jing Cao, Linghui Lu, Chun Li, Peng Wei, Qiyan Wang and Yong Wang
Molecules 2021, 26(5), 1460; https://doi.org/10.3390/molecules26051460 - 08 Mar 2021
Cited by 19 | Viewed by 3121
Abstract
Cardiotoxicity is one of the main side effects of doxorubicin (Dox) treatment. Dox could induce oxidative stress, leading to an opening of the mitochondrial permeability transition pore (mPTP) and apoptosis in cardiomyocytes. Previous studies have shown that Cryptotanshinone (Cts) has potential cardioprotective effects, [...] Read more.
Cardiotoxicity is one of the main side effects of doxorubicin (Dox) treatment. Dox could induce oxidative stress, leading to an opening of the mitochondrial permeability transition pore (mPTP) and apoptosis in cardiomyocytes. Previous studies have shown that Cryptotanshinone (Cts) has potential cardioprotective effects, but its role in Dox-induced cardiotoxicity (DIC) remains unknown. A Dox-stimulated H9C2 cell model was established. The effects of Cts on cell viability, reactive oxygen species (ROS), superoxide ion accumulation, apoptosis and mitochondrial membrane potential (MMP) were evaluated. Expressions of proteins in Akt-GSK-3β pathway were detected by Western blot. An Akt inhibitor was applied to investigate the effects of Cts on the Akt-GSK-3β pathway. The effects of Cts on the binding of p-GSK-3β to ANT and the formation of the ANT-CypD complex were explored by immunoprecipitation assay. The results showed that Cts could increase cell viability, reduce ROS levels, inhibit apoptosis and protect mitochondrial membrane integrity. Cts increased phosphorylated levels of Akt and GSK-3β. After cells were co-treated with an Akt inhibitor, the effects of Cts were abolished. An immunoprecipitation assay showed that Cts significantly increased GSK-3β-ANT interaction and attenuated Dox-induced formation of the ANT-CypD complex, thereby inhibiting opening of the mPTP. In conclusion, Cts could ameliorate oxidative stress and apoptosis via the Akt-GSK-3β-mPTP pathway. Full article
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