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Cardiotoxicity of Chemotherapeutic Agents

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 (31 May 2022) | Viewed by 3349

Special Issue Editor


E-Mail Website1 Website2
Guest Editor
1.Grupo de investigación cardiovascular del Hospital Clínico Universitario de Santiago de Compostela (CardioCHUS), A Coruña, Spain
2.Centro de Investigación Biomédica en Red en Enfermedades Cardiovasculares (CIBERCV), Madrid, Spain
3.Centro de Investigación en Medicina Molecular y Enfermedades Crónicas (CIMUS) , Santiago de Compostela, Spain
Interests: cardiotoxicity; biomarkers; microRNA; cardiac imaging

Special Issue Information

Dear Colleagues,

Continuous advances in the early detection and treatment of cancer have increased overall survival in recent decades. However, it is now well-established that cancer patients and long-term survivors face an increased cardiovascular (CV) morbimortality associated with chemotherapeutic agents. Cardiotoxicity (CT) is currently recognized as a main side effect of chemotherapy. Left ventricular (LV) dysfunction and/or heart failure (HF) are the most common cardiovascular complications after the administration of chemotherapies. As HF may limit optimal cancer treatment, the early detection of myocardial dysfunction during chemotherapy is a major issue. The current context demands greater efforts in clinical and basic research to improve our understanding of the etiopathology of CT. In-depth knowledge of CT-associated pathophysiological mechanisms will allow a suitable cardiovascular risk stratification of cancer patients to be established and early diagnosis tools and novel cardioprotective strategies to be identified.

This Special Issue intends to provide the reader with a better understand of the relationship between cancer therapies and CV toxicity. Overall, we are confident that this Special Issue will be of interest to the scientific community and will help to expand our current knowledge on chemotherapy-associated cardiotoxicity.

Dr. Ricardo Lage Fernández
Guest Editor

Manuscript Submission Information

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Keywords

  • cardiotoxicity
  • chemotherapy
  • biomarkers
  • cardiac imaging
  • global longitudinal strain
  • heart failure

Published Papers (1 paper)

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Research

16 pages, 2378 KiB  
Article
Venetoclax Induces Cardiotoxicity through Modulation of Oxidative-Stress-Mediated Cardiac Inflammation and Apoptosis via NF-κB and BCL-2 Pathway
by Abdullah F. AlAsmari, Adel Alghamdi, Nemat Ali, Muath A. Almeaikl, Hassan M. Hakami, Meshal K. Alyousef, Mohammed AlSwayyed, Metab Alharbi, Faleh Alqahtani, Fawaz Alasmari and Nasser Alsaleh
Int. J. Mol. Sci. 2022, 23(11), 6260; https://doi.org/10.3390/ijms23116260 - 2 Jun 2022
Cited by 6 | Viewed by 2878
Abstract
Cardiovascular damage induced by anticancer therapy has become the main health problem after tumor elimination. Venetoclax (VTX) is a promising novel agent that has been proven to have a high efficacy in multiple hematological diseases, especially acute myeloid leukemia (AML) and chronic lymphocytic [...] Read more.
Cardiovascular damage induced by anticancer therapy has become the main health problem after tumor elimination. Venetoclax (VTX) is a promising novel agent that has been proven to have a high efficacy in multiple hematological diseases, especially acute myeloid leukemia (AML) and chronic lymphocytic leukemia (CLL). Considering its mechanism of action, the possibility that VTX may cause cardiotoxicity cannot be ruled out. Therefore, this study was designed to investigate the toxic effect of VTX on the heart. Male Sprague-Dawley rats were randomly divided into three groups: control, low-dose VTX (50 mg/kg via oral gavage), and high-dose VTX (100 mg/kg via oral gavage). After 21 days, blood and tissue samples were collected for histopathological, biochemical, gene, and protein analyses. We demonstrated that VTX treatment resulted in cardiac damages as evidenced by major changes in histopathology and markedly elevated cardiac enzymes and hypertrophic genes markers. Moreover, we observed a drastic increase in oxidative stress, as well as inflammatory and apoptotic markers, with a remarkable decline in the levels of Bcl-2. To the best of our knowledge, this study is the first to report the cardiotoxic effect of VTX. Further experiments and future studies are strongly needed to comprehensively understand the cardiotoxic effect of VTX. Full article
(This article belongs to the Special Issue Cardiotoxicity of Chemotherapeutic Agents)
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