Oxidative stress and inflammation: determinants of anthracycline cardiotoxicity and possible therapeutic targets

Fabiani, Iacopo; Aimo, Alberto; Grigoratos, Chrysanthos; Castiglione, Vincenzo; Gentile, Francesco; Saccaro, Luigi Francesco; Arzilli, Chiara; Cardinale, Daniela; Passino, Claudio; Emdin, Michele

doi:10.1007/s10741-020-10063-9

Cited by 57 publications

(38 citation statements)

References 86 publications

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“…12 The overproduction of ROS can not only cause cell damage but also amplify inflammation. 13 Activated Kupffer cells secrete inflammatory cytokines, such as tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6), which recruit both neutrophils and macrophages to expand the inflammatory response. 14−16 Therefore, an effective method that is focused on scavenging ROS and regulating inflammation should be employed to protect against AILI.…”

Section: Introductionmentioning

confidence: 99%

Prussian Blue Nanozymes Prevent Anthracycline-Induced Liver Injury by Attenuating Oxidative Stress and Regulating Inflammation

Bai

Kong

Feng

et al. 2021

ACS Appl. Mater. Interfaces

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Anthracycline-induced liver injury (AILI) is becoming an increasingly serious and potential clinical complication and is linked to reactive oxygen species (ROS) production and subsequent inflammatory response. Herein, we demonstrated that artificial Prussian blue nanozymes (PBZs) prevented daunorubicin-induced liver injury, a prototype of AILI, by attenuating ROS production and regulating inflammation. PBZs exhibited multienzyme activity and could scavenge ROS and free radicals. At the cellular level, PBZs could effectively eliminate ROS, suppress hepatocyte apoptosis, reduce deoxyribonucleic acid damage, and decrease the levels of inflammatory cytokines and chemokines. According to the results of the in vivo study, pretreatment with PBZs also resulted in a desirable protective effect against AILI, as indicated by both a decrease in biochemical indicator levels and hepatocyte necrosis. PBZs upregulated antioxidative genes by activating the Nrf2 pathway to reduce oxidative stress. Meanwhile, PBZs counteracted the inflammatory response based on the decreased expression levels of myeloperoxidase and F4/80 in the liver. Collectively, our findings indicate that PBZ-based nanotherapy is a novel strategy for protecting against AILI.

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Section: Introductionmentioning

confidence: 99%

Prussian Blue Nanozymes Prevent Anthracycline-Induced Liver Injury by Attenuating Oxidative Stress and Regulating Inflammation

Bai

Kong

Feng

et al. 2021

ACS Appl. Mater. Interfaces

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“…However, it is still unclear whether these antioxidants exert cardioprotective effects in humans without impairing the anticancer activity of ANTs; moreover, most of these studies evaluated the effects of ANTs alone, not in combination with other therapies. Therefore, larger multicenter trials are required to effectively evaluate the beneficial activity of antioxidant agents in co-administration with ANTs and other anticancer drugs [128,129].…”

Section: Anthracyclines (Ants)mentioning

confidence: 99%

Mitochondrial Determinants of Anti-Cancer Drug-Induced Cardiotoxicity

et al. 2022

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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 targets as major determinants of the cardiotoxic effects triggered by an increasing number of chemotherapeutic agents used for both solid and hematological tumors. Mitochondrial toxicity induced by such anticancer therapeutics is due to different mechanisms, generally altering the mitochondrial respiratory chain, energy production, and mitochondrial dynamics, or inducing mitochondrial oxidative/nitrative stress, eventually culminating in cell death. The present review summarizes key mitochondrial processes mediating the cardiotoxic effects of anti-neoplastic drugs, with a specific focus on anthracyclines (ANTs), receptor tyrosine kinase inhibitors (RTKIs) and proteasome inhibitors (PIs).

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“…Direct infiltration of immune cells may also be a cause of cardiomyopathy [85]. Inflammation is also a hallmark of cardiotoxicity arising from anthracycline therapy [88]. The inflammatory response may be evident shortly after cardiac injury [85].…”

Section: Inflammationmentioning

confidence: 99%

PET Tracers for Imaging Cardiac Function in Cardio-oncology

Kelly

Babich

2022

Curr Cardiol Rep

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Purpose of Review Successful treatment of cancer can be hampered by the attendant risk of cardiotoxicity, manifesting as cardiomyopathy, left ventricle systolic dysfunction and, in some cases, heart failure. This risk can be mitigated if the injury to the heart is detected before the onset to irreversible cardiac impairment. The gold standard for cardiac imaging in cardio-oncology is echocardiography. Despite improvements in the application of this modality, it is not typically sensitive to sub-clinical or early-stage dysfunction. We identify in this review some emerging tracers for detecting incipient cardiotoxicity by positron emission tomography (PET). Recent Findings Vectors labeled with positron-emitting radionuclides (e.g., carbon-11, fluorine-18, gallium-68) are now available to study cardiac function, metabolism, and tissue repair in preclinical models. Many of these probes are highly sensitive to early damage, thereby potentially addressing the limitations of current imaging approaches, and show promise in preliminary clinical evaluations. Summary The overlapping pathophysiology between cardiotoxicity and heart failure significantly expands the number of imaging tools available to cardio-oncology. This is highlighted by the emergence of radiolabeled probes targeting fibroblast activation protein (FAP) for sensitive detection of dysregulated healing process that underpins adverse cardiac remodeling. The growth of PET scanner technology also creates an opportunity for a renaissance in metabolic imaging in cardio-oncology research.

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Oxidative stress and inflammation: determinants of anthracycline cardiotoxicity and possible therapeutic targets

Cited by 57 publications

References 86 publications

Prussian Blue Nanozymes Prevent Anthracycline-Induced Liver Injury by Attenuating Oxidative Stress and Regulating Inflammation

Prussian Blue Nanozymes Prevent Anthracycline-Induced Liver Injury by Attenuating Oxidative Stress and Regulating Inflammation

Mitochondrial Determinants of Anti-Cancer Drug-Induced Cardiotoxicity

PET Tracers for Imaging Cardiac Function in Cardio-oncology

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