Mitochondrial-Targeted Therapy for Doxorubicin-Induced Cardiotoxicity

Wu, Binbin; Leung, Kam Tong; Poon, Ellen

doi:10.3390/ijms23031912

Cited by 52 publications

(28 citation statements)

References 216 publications

(263 reference statements)

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“…Several mechanisms may be responsible for doxorubicin-induced cardiotoxicity. These mechanisms include mitochondrial injury, ROS generation, intracellular Ca+2 dysregulation, inflammatory cytokine production, and myocyte damage ( Rawat et al, 2021 ; Sheibani et al, 2022 ; Wu et al, 2022 ).…”

Section: Discussionmentioning

confidence: 99%

Cardioprotective Effect of Rheum turkestanicum Against Doxorubicin-Induced Toxicity in Rats

et al. 2022

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Background: Doxorubicin as an anti-cancer drug causes cardiotoxicity, limiting its tolerability and use. The mechanism of toxicity is due to free radical production and cardiomyocytes injury. This research evaluated Rheum turkestanicum (R.turkestanicum) extract against doxorubicin cardiotoxicity due to its considerable in vitro antioxidant activity.Methods: Male Wistar rats received 2.5 mg/kg doxorubicin intraperitoneally every other day for 2 weeks to create an accumulative dose. R. turkestanicum was administrated at a dose of 100 and 300 mg/kg intraperitoneally from the second week for 7 days. On the 15th day, the animals were anesthetized and blood was collected from cardiac tissue for evaluation of alanine aminotransferase (ALT), cardiac muscle creatinine kinase (CK-MB), troponin T (cTn-T), lactate dehydrogenase (LDH), and B-type natriuretic peptide brain natriuretic peptide. A cardiac homogenate was also collected to determine superoxide dismutase (SOD), catalase Catalase Activity, malondialdehyde (MDA), and thiols. Histopathology was also performed.Results: Doxorubicin increased all cardiac enzymes and malondialdehyde, correlating with a reduction in SOD, catalase, and thiols. Histopathology revealed extracellular edema, moderate congestion, and hemorrhage of foci. In contrast, administration of R. turkestanicum ameliorated these doxorubicin-induced pathophysiological changes.Conclusion: This study revealed that the extract ameliorated doxorubicin-induced cardiac toxicity via modulation of oxidative stress-related pathways. Liquid chromatography-mass spectrometry analysis of R. turkestanicum indicated several components with potent pharmacological properties.

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Section: Discussionmentioning

confidence: 99%

Cardioprotective Effect of Rheum turkestanicum Against Doxorubicin-Induced Toxicity in Rats

et al. 2022

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“…DOX treatment in patients shows both effects like therapeutic and toxic effects. It has been reported that the cardiomyopathy initiated by doxorubicin is a progressive and multifactorial process (Wu et al, 2022), including oxidative stress, iron accumulation with the alteration of gene and protein expression and DNA breakage via inhibition of topoisomerase II (Kong et al, 2022).…”

Section: Advances Inmentioning

confidence: 99%

Terminalia muelleri Attenuates the Accumulation of Excess Iron, Inhibition of Topoisomerase 2ß and Oxidative Cardiac Damage in Doxorubicin-Induced Cardiotoxicity in Rats

Eltablawy¹,

Sayed²,

Barry³

et al. 2022

AAVS

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C ardiovascular system dysfunction is one of the most frequent consequences of exposure to antineoplastic treatment, whereas cardiovascular diseases and cancers are the leading causes of morbidity and mortality in the world (Sung et al., 2021). The less regeneration ability of cardi-ac cells renders cardiac myocytes to be more prone to the long-term adverse effects of chemotherapy agents such as anthracycline (Hardaway, 2019).Cardiotoxicity is the toxicity that affects the heart. This definition is attributed to the effect of chemotherapy on the entire cardiovascular system that occurs through di-

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“…Unfortunately, since this activity is aspecific, severe adverse reactions against non-targeted tissues/organs have been observed. Indeed, dose-dependent cardiotoxicity and myelosuppression are the most common limiting effects of DOX administration [ 6 , 7 ]. Another important issue is related to the appearance of chemoresistant cell lines, a phenomenon caused by the upregulation of drug efflux transporters or epigenetic modifications [ 8 , 9 ].…”

Section: Introductionmentioning

confidence: 99%

Gliadin Nanoparticles Containing Doxorubicin Hydrochloride: Characterization and Cytotoxicity

et al. 2023

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Doxorubicin hydrochloride (DOX) is a well-known antitumor drug used as first line treatment for many types of malignancies. Despite its clinical relevance, the administration of the compound is negatively affected by dose-dependent off-target toxicity phenomena. Nanotechnology has helped to overcome these important limitations by improving the therapeutic index of the bioactive and promoting the translation of novel nanomedicines into clinical practice. Herein, nanoparticles made up of wheat gliadin and stabilized by polyoxyethylene (2) oleyl ether were investigated for the first time as carriers of DOX. The encapsulation of the compound did not significantly affect the physico-chemical features of the gliadin nanoparticles (GNPs), which evidenced a mean diameter of ~180 nm, a polydispersity index < 0.2 and a negative surface charge. The nanosystems demonstrated great stability regarding temperature (25–50 °C) and were able to retain high amounts of drug, allowing its prolonged and sustained release for up to a week. In vitro viability assay performed against breast cancer cells demonstrated that the nanoencapsulation of DOX modulated the cytotoxicity of the bioactive as a function of the incubation time with respect to the free form of the drug. The results demonstrate the potential use of GNPs as carriers of hydrophilic antitumor compounds.

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Mitochondrial-Targeted Therapy for Doxorubicin-Induced Cardiotoxicity

Cited by 52 publications

References 216 publications

Cardioprotective Effect of Rheum turkestanicum Against Doxorubicin-Induced Toxicity in Rats

Cardioprotective Effect of Rheum turkestanicum Against Doxorubicin-Induced Toxicity in Rats

Terminalia muelleri Attenuates the Accumulation of Excess Iron, Inhibition of Topoisomerase 2ß and Oxidative Cardiac Damage in Doxorubicin-Induced Cardiotoxicity in Rats

Gliadin Nanoparticles Containing Doxorubicin Hydrochloride: Characterization and Cytotoxicity

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