Why the study?
Doxorubicin is an effective anticancer agent associated with cardiotoxic side effects in some patients, with mitochondrial damage implicated as a key pathogenesis of myocardial injury.
Does mitochondrial transplantation improve cardiac function and reduce cardiotoxicity in doxorubicin-treated models?
Does mitochondrial transplantation improve cardiac function and reduce cardiotoxicity in doxorubicin-treated models?
Mitochondrial transplantation from various sources, including arterial blood, may serve as a potential therapeutic strategy for doxorubicin-induced cardiotoxicity by activating glutamine metabolism.
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Mitochondrial transplantation may attenuate doxorubicin cardiotoxicity in preclinical models; leaves open clinical translation and efficacy.
Sun et al. (2023) studied this question.
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