Pathophysiology of Doxorubicin-Mediated Cardiotoxicity DOI Creative Commons
Roberto Arrigoni, Emilio Jirillo, Carlo Caiati

et al.

Toxics, Journal Year: 2025, Volume and Issue: 13(4), P. 277 - 277

Published: April 5, 2025

Doxorubicin (DOX) is used for the treatment of various malignancies, including leukemias, lymphomas, sarcomas, and bladder, breast, gynecological cancers in adults, adolescents, children. However, DOX causes severe side effects patients, such as cardiotoxicity, which encompasses heart failure, arrhythmia, myocardial infarction. DOX-induced cardiotoxicity (DIC) based on combination nuclear-mediated cardiomyocyte death mitochondrial-mediated death. Oxidative stress, altered autophagy, inflammation, apoptosis/ferroptosis represent main pathogenetic mechanisms responsible DIC. In addition, vitro vivo models DIC sirtuins (SIRT), especially, SIRT 1 are reduced, this event contributes to cardiac damage. fact, inhibits reactive oxygen species NF-kB activation, thus improving oxidative stress remodeling. Therefore, recovery during may a therapeutic strategy limit progression. Natural products, i.e., polyphenols, well nano formulations iron chelators, other potential compounds experimented with At present, few clinical trials available confirm efficacy these products The aim review description pathophysiology drug targets alleviate

Language: Английский

Pathophysiology of Doxorubicin-Mediated Cardiotoxicity DOI Creative Commons
Roberto Arrigoni, Emilio Jirillo, Carlo Caiati

et al.

Toxics, Journal Year: 2025, Volume and Issue: 13(4), P. 277 - 277

Published: April 5, 2025

Doxorubicin (DOX) is used for the treatment of various malignancies, including leukemias, lymphomas, sarcomas, and bladder, breast, gynecological cancers in adults, adolescents, children. However, DOX causes severe side effects patients, such as cardiotoxicity, which encompasses heart failure, arrhythmia, myocardial infarction. DOX-induced cardiotoxicity (DIC) based on combination nuclear-mediated cardiomyocyte death mitochondrial-mediated death. Oxidative stress, altered autophagy, inflammation, apoptosis/ferroptosis represent main pathogenetic mechanisms responsible DIC. In addition, vitro vivo models DIC sirtuins (SIRT), especially, SIRT 1 are reduced, this event contributes to cardiac damage. fact, inhibits reactive oxygen species NF-kB activation, thus improving oxidative stress remodeling. Therefore, recovery during may a therapeutic strategy limit progression. Natural products, i.e., polyphenols, well nano formulations iron chelators, other potential compounds experimented with At present, few clinical trials available confirm efficacy these products The aim review description pathophysiology drug targets alleviate

Language: Английский

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