Primary Prevention Strategies for Anthracycline Cardiotoxicity: A Brief Overview

Menna, Pierantonio; Salvatorelli, Emanuela

doi:10.1159/000455823

Cited by 67 publications

(57 citation statements)

References 61 publications

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“…Although various cancer immunotherapies have emerged (Wang, 2017), chemotherapy remains one of the most effective treatments for advanced cancers (Benevento et al, 2017;Menna and Salvatorelli, 2017). However, chemotherapeutic drugs usually cause immunosuppression, which impairs their antitumor effects.…”

Section: Discussionmentioning

confidence: 99%

Specific Decrease in B-Cell-Derived Extracellular Vesicles Enhances Post-Chemotherapeutic CD8+ T Cell Responses

et al. 2019

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Graphical Abstract Highlights d CD19 + EVs through CD39 and CD73 hydrolyze ATP from tumor cells into adenosine d CD19 + EVs blunt post-chemotherapeutic CD8 T cell responses via adenosine d Tumor B cells produce more EVs by enhancing HIF-1a-mediated Rab27a transcription d IEBVs-Rab27a siRNA is a potential tool for improving chemotherapeutic effect SUMMARY Systemic immunosuppression greatly affects the chemotherapeutic antitumor effect. Here, we showed that CD19 + extracellular vesicles (EVs) from B cells through CD39 and CD73 vesicle-incorporated proteins hydrolyzed ATP from chemotherapy-treated tumor cells into adenosine, thus impairing CD8 + T cell responses. Serum CD19 + EVs were increased in tumor-bearing mice and patients. Patients with fewer serum CD19 + EVs had a better prognosis after chemotherapy. Upregulated hypoxia-inducible factor-1a (HIF-1a) promoted B cells to release CD19 + EVs by inducing Rab27a mRNA transcription. Rab27a or HIF-1a deficiency in B cells inhibited CD19 + EV production and improved the chemotherapeutic antitumor effect. Silencing of Rab27a in B cells by inactivated Epstein-Barr viruses carrying Rab27a siRNA greatly improved chemotherapeutic efficacy in humanized immunocompromised NOD Prkdc scid Il2rg À/À mice. Thus, decreasing CD19 + EVs holds high potential to improve the chemotherapeutic antitumor effect.

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Section: Discussionmentioning

confidence: 99%

Specific Decrease in B-Cell-Derived Extracellular Vesicles Enhances Post-Chemotherapeutic CD8+ T Cell Responses

et al. 2019

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“…Anthracyclines, including doxorubicin, epirubicin, daunourubicin, and idarubicin, play a major role in chemotherapy and are used to treat many solid organ tumours and haematologic malignancies such as breast, ovarian, lung, uterine, and bladder cancers, and different types of leukaemias and lymphomas [28,29]. However, it is widely reported that dose-dependent cardiotoxicity of anthracyclines limit their clinical effectiveness [1-4, 28, 29].…”

Section: Discussionmentioning

confidence: 99%

Cardioprotective Potential of Murraya koenigii (L.) Spreng. Leaf Extract against Doxorubicin‐Induced Cardiotoxicity in Rats

Sandamali

Hewawasam

Jayatilaka

et al. 2020

Evidence-Based Complementary and Alternative Medicine

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Dose-dependent cardiotoxicity of doxorubicin may lead to irreversible congestive heart failure. Although multiple mechanisms are involved, generation of free radicals is the most commonly postulated mechanism. erefore, free radical scavengers are considered as potential therapeutic agents. As Murraya koenigii leaves are a rich source of flavonoids and phenols, they have the ability to scavenge free radicals effectively. erefore, the objective of this study was to investigate the cardioprotective potential of Murraya leaf extract against doxorubicin-induced cardiotoxicity in rats. Rats were randomly divided into five groups with 10 animals in each group. Doxorubicin was administered intraperitonially at 18 mg/kg while lyophilized plant extract was administered orally at 2 g/kg. Dexrazoxane, at 180 mg/kg, was used as the positive control. Cardiac damage of doxorubicin control was evident with a significant increase (p < 0.05) in cardiac troponin I, NT-pro BNP, AST, and LDH compared to the normal control. Plant-treated group showed cardioprotective effect by significantly reducing (p < 0.05) all of the above parameters compared to doxorubicin control (p < 0.05). Increased oxidative stress in doxorubicin control was evident with a significant reduction in reduced glutathione, glutathione reductase, glutathione peroxidase, total antioxidant capacity, superoxide dismutase, and catalase activity and a significant increase in lipid peroxidation compared to the control. Interestingly, treatment with Murraya leaf extract showed a significant increase in all of the above antioxidant parameters and a significant reduction in lipid peroxidation by showing an antioxidant effect. A significant increase in myeloperoxidase activity confirmed the increased inflammatory activity in doxorubicin control group whereas plant-treated group showed a significant reduction (p < 0.05) which expressed the anti-inflammatory effect of Murraya leaf extract. Doxorubicin-treated group showed histological evidence of extensive damage to the myocardium while plant-treated group showed a preserved myocardium with lesser degree of damage. Pretreatment with Murraya leaf extract may replenish cardiomyocytes with antioxidants and promote the defense against doxorubicin-induced cardiotoxicity.

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“…Cardioprotective Agents Against Anthracycline -Induced Cardiotoxicity: Drugs used clinically for prevention of anthracycline (doxorubicin) induced toxicity are shown in Table 2. Unfortunately, none of the drugs till date is clinically established as a cardioprotective agent against anthracycline (doxorubicin -induced toxicity) 22 .…”

Section: 2mentioning

confidence: 99%

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2018

IJPSR

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Cardiotoxicity associated with the clinically used drugs is a global concern of safety for healthcare professionals. Various animal models have been used to study the drug-induced cardiotoxicity but the exact molecular involvement of toxicity is not much clear. Despite the recurrent occurrence of toxicities, drugs such as doxorubicin, calcium channel blockers, antiarrhythmics and immunomodulators are regularly used. Anticancer drugs mainly anthracyclines, 5-fluorouracil and cyclophosphamide exert prominent cardiotoxicity. Till date, there is only one drug approved for doxorubicin-related cardiotoxicity i.e. dexrazoxane. Few other drugs are used routinely by clinicians to reduce the severity of toxicity which includes ACE inhibitors, L-carnitine, probucol, CoQ 10 , N-acetylcysteine, Vitamin E and deferoxamine, whereas antidepressants drugs, specifically tricyclic antidepressants are potential candidates for cardiotoxicity. Calcium channel blockers, antiarrhythmic and beta receptor antagonist aggravate cardiac heart failure (CHF) and left ventricular arrhythmia. Interferons, mainly interferon-α is also associated with prominent and dose-dependant toxicity. Some other drugs like zidovudine, chloroquine, cocaine, minoxidil, ketoconazole, prostaglandin E2 and anagrelide are also reported to have cardiotoxic effects. A complication associated with the use of these drugs include hypoxia, coronary ischemia, calcium overload, oxidative stress, contractile dysfunction, left ventricular arrhythmia and cardiomyopathy.

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Primary Prevention Strategies for Anthracycline Cardiotoxicity: A Brief Overview

Cited by 67 publications

References 61 publications

Specific Decrease in B-Cell-Derived Extracellular Vesicles Enhances Post-Chemotherapeutic CD8+ T Cell Responses

Specific Decrease in B-Cell-Derived Extracellular Vesicles Enhances Post-Chemotherapeutic CD8+ T Cell Responses

Cardioprotective Potential of Murraya koenigii (L.) Spreng. Leaf Extract against Doxorubicin‐Induced Cardiotoxicity in Rats

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