Drug-Induced Cardiotoxicity 2023

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

Deadline for manuscript submissions: closed (30 June 2023) | Viewed by 3972

Special Issue Editor

Department of Invasive Cardiology, Centre of Postgraduate Medical Education, Woloska Street 137, 02-507 Warsaw, Poland
Interests: coronary microcirculation dysfunction; coronary artery bifurcation stenting; statins; cardiotoxicity; statins antitumor activity
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Dear Colleagues,

In recent years, the cardiotoxicity of cancer treatments has been a topic of growing interest, and an entirely new branch has developed, i.e., cardio-oncology. In 2020, the European Society of Cardiology issued the first cardio-oncology guidelines. Nevertheless, many aspects of cancer drug-induced cardiovascular diseases remain not fully elucidated.

Recent evidence suggests that cardiac dysfunction and subsequent heart failure are mainly due to vascular toxicity rather than only due to myocyte toxicity. However, not all vascular toxicity of cancer therapies can be explained by epicardial coronary artery disease. In recent decades, it has been revealed that myocardial ischemia may occur because of structural or functional dysfunction in the complex network of coronary microcirculation vessels.

We invite authors to submit original studies, reviews, meta-analyses, and case reports focused on drug-induced cardiotoxicity showing common pathophysiologic mechanisms, proposing new diagnostic approaches and therapeutic options for cardioprotection. We are soliciting not only human studies but animal and molecular studies as well.

Dr. Jacek Bil
Guest Editor

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Keywords

  • cardiooncology
  • heart failure
  • microcirculation
  • treatment complications

Published Papers (2 papers)

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Research

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19 pages, 6144 KiB  
Article
Exposure to Doxorubicin Modulates the Cardiac Response to Isoproterenol in Male and Female Mice
by Kevin Agostinucci, Marianne K. O. Grant, Wongel Melaku, Chandini Nair and Beshay N. Zordoky
Pharmaceuticals 2023, 16(3), 391; https://doi.org/10.3390/ph16030391 - 04 Mar 2023
Cited by 3 | Viewed by 1937
Abstract
Sex is a salient risk factor in the development of doxorubicin-induced cardiotoxicity. Sex differences in the heart’s ability to respond to hypertrophic stimuli in doxorubicin-exposed animals have not been reported. We identified the sexual dimorphic effects of isoproterenol in mice pre-exposed to doxorubicin. [...] Read more.
Sex is a salient risk factor in the development of doxorubicin-induced cardiotoxicity. Sex differences in the heart’s ability to respond to hypertrophic stimuli in doxorubicin-exposed animals have not been reported. We identified the sexual dimorphic effects of isoproterenol in mice pre-exposed to doxorubicin. Male and female intact or gonadectomized C57BL/6N mice underwent five weekly intraperitoneal injections of 4 mg/kg doxorubicin followed by a five-week recovery period. Fourteen days of subcutaneous isoproterenol injections (10 mg/kg/day) were administered after the recovery period. Echocardiography was used to assess heart function one and five weeks after the last doxorubicin injection and on the fourteenth day of isoproterenol treatment. Thereafter, mice were euthanized, and the hearts were weighed and processed for histopathology and gene expression analysis. Doxorubicin did not produce overt cardiac dysfunction in male or female mice before starting isoproterenol treatment. The chronotropic response to a single isoproterenol injection was blunted by doxorubicin, but the inotropic response was maintained in both males and females. Pre-exposure to doxorubicin caused cardiac atrophy in both control and isoproterenol-treated male mice but not in female mice. Counterintuitively, pre-exposure to doxorubicin abrogated isoproterenol-induced cardiac fibrosis. However, there were no sex differences in the expression of markers of pathological hypertrophy, fibrosis, or inflammation. Gonadectomy did not reverse the sexually dimorphic effects of doxorubicin. Additionally, pre-exposure to doxorubicin abrogated the hypertrophic response to isoproterenol in castrated male mice but not in ovariectomized female mice. Therefore, pre-exposure to doxorubicin caused male-specific cardiac atrophy that persisted after isoproterenol treatment, which could not be prevented by gonadectomy. Full article
(This article belongs to the Special Issue Drug-Induced Cardiotoxicity 2023)
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25 pages, 2567 KiB  
Review
Recent Perspectives on Cardiovascular Toxicity Associated with Colorectal Cancer Drug Therapy
by Monu Kumar Kashyap, Shubhada V. Mangrulkar, Sapana Kushwaha, Akash Ved, Mayur B. Kale, Nitu L. Wankhede, Brijesh G. Taksande, Aman B. Upaganlawar, Milind J. Umekar, Sushruta Koppula and Spandana Rajendra Kopalli
Pharmaceuticals 2023, 16(10), 1441; https://doi.org/10.3390/ph16101441 - 11 Oct 2023
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Abstract
Cardiotoxicity is a well-known adverse effect of cancer-related therapy that has a significant influence on patient outcomes and quality of life. The use of antineoplastic drugs to treat colorectal cancers (CRCs) is associated with a number of undesirable side effects including cardiac complications. [...] Read more.
Cardiotoxicity is a well-known adverse effect of cancer-related therapy that has a significant influence on patient outcomes and quality of life. The use of antineoplastic drugs to treat colorectal cancers (CRCs) is associated with a number of undesirable side effects including cardiac complications. For both sexes, CRC ranks second and accounts for four out of every ten cancer deaths. According to the reports, almost 39% of patients with colorectal cancer who underwent first-line chemotherapy suffered cardiovascular impairment. Although 5-fluorouracil is still the backbone of chemotherapy regimen for colorectal, gastric, and breast cancers, cardiotoxicity caused by 5-fluorouracil might affect anywhere from 1.5% to 18% of patients. The precise mechanisms underlying cardiotoxicity associated with CRC treatment are complex and may involve the modulation of various signaling pathways crucial for maintaining cardiac health including TKI ErbB2 or NRG-1, VEGF, PDGF, BRAF/Ras/Raf/MEK/ERK, and the PI3/ERK/AMPK/mTOR pathway, resulting in oxidative stress, mitochondrial dysfunction, inflammation, and apoptosis, ultimately damaging cardiac tissue. Thus, the identification and management of cardiotoxicity associated with CRC drug therapy while minimizing the negative impact have become increasingly important. The purpose of this review is to catalog the potential cardiotoxicities caused by anticancer drugs and targeted therapy used to treat colorectal cancer as well as strategies focused on early diagnosing, prevention, and treatment of cardiotoxicity associated with anticancer drugs used in CRC therapy. Full article
(This article belongs to the Special Issue Drug-Induced Cardiotoxicity 2023)
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