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2-Hydroxyanthraquinone induces cardiotoxicity in zebrafish via ferroptosis.

2-Hydroxyanthraquinone (2-hATQ) is a photochemical oxidation product of anthracene (ANT), a polycyclic aromatic hydrocarbon. ANT is listed as a priority pollutant by the US Environmental Protection Agency (EPA) due to its resistance to degradation and persistence in the environment. Because of ANT's characteristics, 2-hATQ can also be ubiquitously present in the environment and is more toxic than its parent compound ANT, posing significant risks to environmental safety and human health. Nevertheless, there are limited studies addressing its toxicological effects, particularly concerning cardio

Post-transplant cyclophosphamide-induced cardiotoxicity: A comprehensive review.

Cyclophosphamide-induced cardiotoxicity, associated with its toxic metabolite acrolein, is a significant concern and unresolved issue, especially when cyclophosphamide is administrated in high doses. However, cardiotoxicity following low-dose cyclophosphamide has been also documented, especially in post-hematopoietic stem cell transplantation (post-HSCT) settings. Despite the involvement of multiple signaling pathways in cyclophosphamide-induced cardiomyopathy, the exact underlying mechanisms remain to be fully elucidated. This review outlines the current challenges of cyclophosphamide therapy…

Cardiotoxicity of chloroquine and hydroxychloroquine through mitochondrial pathway.

BACKGROUND: Medical therapies can cause cardiotoxicity. Chloroquine (QC) and hydroxychloroquine (HQC) are drugs used in the treatment of malaria and skin and rheumatic disorders. These drugs were considered to help treatment of coronavirus disease (COVID-19) in 2019. Despite the low cost and availability of QC and HQC, reports indicate that this class of drugs can cause cardiotoxicity. The mechanism of this event is not well known, but evidence shows that QC and HQC can cause cardiotoxicity by affecting mitochondria and lysosomes. METHODS: Therefore, our study was designed to investigate the …

Radiation Treatment Mechanisms of Cardiotoxicity: A Systematic Review.

Radiotherapy may be used alone or in combination with chemotherapy for cancer treatment. There are many mechanisms of radiation treatment exposure to toxicities. Our aim was to summarize the literature about known mechanisms of radiation-induced cardiac toxicities. We performed a systematic review of the literature on the PubMed database until October 2022 about cardiovascular toxicities and radiation therapy exposure. Only systematic reviews, meta-analyses, and reviews were selected. Out of 1429 publications screened, 43 papers met inclusion criteria and were selected for the umbrella review

Unexpected worsening of doxorubicin cardiotoxicity upon intermittent fasting.

Recently in Cell Metabolism, Ozcan et al. used preclinical and clinical data to suggest that alternate-day fasting may exacerbate the cardiotoxic effects of doxorubicin through the TFEB/GDF15 pathway, leading to myocardial atrophy and impaired cardiac function. The link between caloric intake, chemotherapy-induced cachexia, and cardiotoxicity warrants more clinical attention.

Apolipoprotein M Attenuates Anthracycline Cardiotoxicity and Lysosomal Injury.

Apolipoprotein M (ApoM) binds sphingosine-1-phosphate (S1P) and is inversely associated with mortality in human heart failure (HF). Here, we show that anthracyclines such as doxorubicin (Dox) reduce circulating ApoM in mice and humans, that ApoM is inversely associated with mortality in patients with anthracycline-induced heart failure, and ApoM heterozygosity in mice increases Dox-induced mortality. In the setting of Dox stress, our studies suggest ApoM can help sustain myocardial autophagic flux in a post-transcriptional manner, attenuate Dox cardiotoxicity, and prevent lysosomal injury.

Mitochondrial Determinants of Anti-Cancer Drug-Induced Cardiotoxicity.

Mitochondria are key organelles for the maintenance of myocardial tissue homeostasis, playing a pivotal role in adenosine triphosphate (ATP) production, calcium signaling, redox homeostasis, and thermogenesis, as well as in the regulation of crucial pathways involved in cell survival. On this basis, it is not surprising that structural and functional impairments of mitochondria can lead to contractile dysfunction, and have been widely implicated in the onset of diverse cardiovascular diseases, including ischemic cardiomyopathy, heart failure, and stroke. Several studies support mitochondrial t

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… In the following paragraphs, we will analyze the main mitochondrial determinants of cardiotoxicity secondary to three major classes of antineoplastic drugs widely reported as cardiotoxic, represented by ANTs, RTKIs and PIs. 3.1. … To overcome the cardiotoxicity of PIs like carfilzomib, mitochondrial functions affected by PIs are being dissected, and novel PIs devoid of cardiotoxicity are also being developed and analyzed in preclinical studies [ 222 ]. …

Colchicine Ameliorates 5-Fluorouracil-Induced Cardiotoxicity in Rats.

Background and Objective. 5-Fluorouracil is one of the most common chemotherapeutic agents used in the treatment of solid tumors. 5-Fluorouracil-associated cardiotoxicity is the second cause of cardiotoxicity induced by chemotherapeutic drugs after anthracyclines. Colchicine is a strong anti-inflammatory drug used to prevent and treat acute gout and treat familial Mediterranean fever. And also, its protective effects on cardiovascular disease have been reported in various studies. The current study is aimed at appraising the effect of colchicine on 5-fluorouracil-induced cardiotoxicity in rats…

Cardiotoxicity linked to anticancer agents and cardioprotective strategy.

Chemotherapy is a main treatment for cancer, and it benefits patients by controlling cancer relapse and metastasis, thereby leading to an increase in the overall survival rate. However, this treatment is associated with mild to severe side effects, one of which is cardiotoxicity. The severity of cardiotoxicity, a leading cause of cardiovascular diseases, depends on the type of cancer therapy employed and the time required for its management. A chemotherapeutic agent is used either alone or in combination with other drugs for cancer treatment. The exact mechanism of chemotherapeutic agent-induc…

Interrelated In Vitro Mechanisms of Sibutramine-Induced Cardiotoxicity.

Consumption of illicit pharmaceutical products containing sibutramine has been reported to cause cardiovascular toxicity problems. This stud … nsistent with the acute inhibition of the repolarizing IK, affecting AP parameters, and provoke the cardiotoxicity.

Cardiotoxicity of cancer chemotherapy: identification, prevention and treatment.

Cardiotoxicity is an important complication of several cancer therapeutic agents. Several well established and newer anticancer therapies such as anthracyclines, trastuzumab and other HER2 receptor blockers, antimetabolites, alkylating agents, tyrosine kinase inhibitors (TKIs), angiogenesis inhibitors, and checkpoint inhibitors are associated with significant cardiotoxicity. Cardiovascular imaging employing radionuclide imaging, echocardiography and magnetic resonance imaging are helpful in early detection and prevention of overt heart failure secondary to cardiotoxicity of cancer therapy. An …

New insights into cardiotoxicity caused by chemotherapeutic agents.

This article is part of a themed section on New Insights into Cardiotoxicity Caused by Chemotherapeutic Agents. To view the other articles in this section visit http://onlinelibrary.wiley.com/doi/10.1111/bph.v174.21/issuetoc.

Cardiotoxicity evaluation of nine alkaloids from Rhizoma Coptis.

PURPOSE: Alkaloids derived from Rhizoma Coptis (RC) has been widely applied to clinical treatments in China. However, the toxicity of RC and … 0 μM. Cytotoxicity was induced by these two compounds with decline in cell index and ATP depletion. Cardiotoxicity or cytotoxicity was not observed in the other five alkaloids within 10 μM. CONCLUSION: For the first time, the cardiotoxicity of the nine alkaloids was evaluated to clarify the cardiotoxic components in RC. Furthermore, the experimental evidences w …

[Cardiotoxicity of trastuzumab: mechanisms of development, diagnosis, treatment].

The review discusses mechanisms of trastuzumab cardio- toxicity. There are presented risk factors of development of the left ventricular dysfunction in treatment of a drug, among which the most important are the simultaneous administration of anthracycline antibiotics and the presence of associated cardiovascular diseases. There are discussed the features of cardiac management of patients receiving trastuzumab therapy that focuses on early detection of abnormalities of left ven- tricular function from the normality as well as measures aim- ing at preventing the occurrence of cardiac dysfunctio

Chloroquine cardiotoxicity mimicking connective tissue disease heart involvement.

The authors report a case of rare chloroquine cardiotoxicity mimicking connective tissue disease heart involvement in a 56-year-old woman with mixed connective tissue disease (MCTD) manifested suddenly as third degree A-V block with QT(c) interval prolongation and short torsade de pointes runs ultimately degenerating into ventricular fibrillation. Immunological tests suggested an MCTD flare, implying that cardiac arrest had resulted from myocardial involvement by MCTD. However, QT(c) prolongation is not a characteristic of cardiomyopathy caused by connective tissue disease, unless anti-Ro/SSA …

5-fluorouracil induced cardiotoxicity: review of the literature.

5-fluorouracil (5-FU) is a key chemotherapeutic agent in the treatment of many gastrointestinal tract adenocarcinomas. Despite its proven therapeutic efficacy, 5-FU also possesses several undesired cardiac toxicities, including coronary vasospasm, coronary thrombosis, cardiomyopathy, and sudden cardiac death. This review addresses the incidence, mechanisms of action, clinical presentation, risk stratification, and management of 5-FU associated cardiotoxicity; it also highlights the importance of careful pre-administration cardiac risk stratification and close monitoring during and after drug a…

Cardiotoxicity associated with trastuzumab in normal clinical practice.

OBJECTIVE: To evaluate the incidence of cardiotoxicity associated with treatment with trastuzumab in clinical practice by describing its characteristics, progress and associated risk factors. METHODS: Retrospective observational study of patients with HER2-positive breast cancer treated with trastuzumab in the fi rst quarter of 2007 in a tertiary hospital. Follow-up was performed from start of treatment until the end of March 2008. The data sources used were the oncological computer program Oncowin® from the pharmacy department and the patient clinical history. We gathered variables related t…

Trastuzumab cardiotoxicity: biological hypotheses and clinical open issues.

BACKGROUND: Trastuzumab has significantly improved the prognosis of breast cancer patients overexpressing the human epidermal growth factor … ies and stress from administration of anthracyclines. This has led to a proposed novel mechanism of cardiotoxicity that appears to be quite different from the anthracycline-associated cardiotoxicity. Trastuzumab does not seem to cause any overt ultrastructural abnormality; it does, however, lead to myocardial dysfunction. CONCLUSION: Most of the proposed hypoth …

Cardiotoxicity of chemotherapeutic agents: incidence, treatment and prevention.

Cytostatic antibiotics of the anthracycline class are the best known of the chemotherapeutic agents that cause cardiotoxicity. Alkylating agents such as cyclophosphamide, ifosfamide, cisplatin, carmustine, busulfan, chlormethine and mitomycin have also been associated with cardiotoxicity. Other agents that may induce a cardiac event include paclitaxel, etoposide, teniposide, the vinca alkaloids, fluorouracil, cytarabine, amsacrine, cladribine, asparaginase, tretinoin and pentostatin. Cardiotoxicity is rare with some agents, but may occur in >20% of patients treated with doxorubicin, daunorubic…