Onco-Cardiologic Aspects of Chronic Heart Failure: Novel Molecular Mechanisms and Pharmacologic Treatment Options

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Cellular Pathology".

Deadline for manuscript submissions: 31 October 2024 | Viewed by 1544

Special Issue Editors


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Guest Editor
Department of Biochemistry, Faculty of Medicine, University of Szeged, Szeged, Hungary
Interests: experimental cardiology; heart failure; uremic cardiomyopathy; onco-cardiology; cardiac ischemia/reperfusion injury; metabolic diseases

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Guest Editor
Department of Pharmacodynamics and Biopharmacy, University of Szeged, Szeged, Hungary
Interests: steroidal anticancer agents; cell cycle blockade; antimetastatic activity; tubulin polymerization; metastasis pathways; HPV-associated cancer
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Special Issue Information

Dear Colleagues,

Cardiovascular diseases and cancer remain the two leading causes of morbidity and mortality worldwide. Better diagnostics and therapeutic tools in cancer management led to increased long-term survival rates among cancer patients. The chronic side effects of cancer therapy frequently aggravate age-related cardiovascular risk factors, leading to late onco-cardiologic complications, such as chronic heart failure in long-term cancer survivors. In addition, several studies showed that localized tumors could affect heart function and result in pathologic cardiac remodeling before the beginning of oncologic treatments. The severity and relevance of cardiovascular risk vary widely depending on the cancer type and cancer treatment regimens. Although the cardiovascular effects of antineoplastic treatment options, including radiotherapy, chemotherapy, and immunotherapy, are receiving more attention, little is known about successful methods for preventing chronic cardiovascular complications in long-term cancer survivors.

The present Special Issue aims to collect and document new findings in the molecular and cellular mechanisms of chronic heart failure and cardiac remodeling induced by anticancer agents, radiotherapy, or tumors. Studies that investigate the effects of pharmacologic agents on the development of anticancer treatments-induced chronic heart failure are welcome to promote and support their application in heart failure therapy.

We invite you to submit original basic research or review articles on the topic of onco-cardiologic aspects of chronic heart failure, with a special focus on novel molecular and cellular mechanisms and pharmacologic treatment options.

Dr. Márta Sárközy
Dr. Renáta Minorics
Guest Editors

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Keywords

  • chronic heart failure
  • cardiac remodeling
  • heart failure therapy
  • cardiovascular diseases
  • cancer management
  • cardiovascular risk factors
  • onco-cardiology

Published Papers (1 paper)

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Research

11 pages, 1661 KiB  
Communication
Pyridoxamine Attenuates Doxorubicin-Induced Cardiomyopathy without Affecting Its Antitumor Effect on Rat Mammary Tumor Cells
by Sibren Haesen, Eline Verghote, Ellen Heeren, Esther Wolfs, Dorien Deluyker and Virginie Bito
Cells 2024, 13(2), 120; https://doi.org/10.3390/cells13020120 - 9 Jan 2024
Cited by 1 | Viewed by 1261
Abstract
Doxorubicin (DOX) is commonly used in cancer treatment but associated with cardiotoxicity. Pyridoxamine (PM), a vitamin B6 derivative, could be a cardioprotectant. This study investigated the effect of PM on DOX cardiotoxicity and DOX antitumor effectiveness. Sprague Dawley rats were treated intravenously with [...] Read more.
Doxorubicin (DOX) is commonly used in cancer treatment but associated with cardiotoxicity. Pyridoxamine (PM), a vitamin B6 derivative, could be a cardioprotectant. This study investigated the effect of PM on DOX cardiotoxicity and DOX antitumor effectiveness. Sprague Dawley rats were treated intravenously with DOX (2 mg/kg/week) or saline over eight weeks. Two other groups received PM via oral intake (1 g/L in water bottles) next to DOX or saline. Echocardiography was performed after eight weeks. PM treatment significantly attenuated the DOX-induced reduction in left ventricular ejection fraction (72 ± 2% vs. 58 ± 3% in DOX; p < 0.001) and increase in left ventricular end-systolic volume (0.24 ± 0.02 µL/cm2 vs. 0.38 ± 0.03 µL/cm2 in DOX; p < 0.0001). Additionally, LA7 tumor cells were exposed to DOX, PM, or DOX and PM for 24 h, 48 h, and 72 h. Cell viability, proliferation, cytotoxicity, and apoptosis were assessed. DOX significantly reduced LA7 cell viability and proliferation (p < 0.0001) and increased cytotoxicity (p < 0.05) and cleaved caspase-3 (p < 0.001). Concomitant PM treatment did not alter the DOX effect on LA7 cells. In conclusion, PM attenuated DOX-induced cardiomyopathy in vivo without affecting the antitumor effect of DOX in vitro, highlighting PM as a promising cardioprotectant for DOX-induced cardiotoxicity. Full article
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