Key result
Kartogenin reduced doxorubicin-induced cardiac insufficiency, myocardial injury, oxidative stress damage, and mitochondrial dysfunction in in vivo and in vitro models.
Why the study?
Does Kartogenin reduce doxorubicin-induced cardiotoxicity in preclinical models?
Does Kartogenin reduce doxorubicin-induced cardiotoxicity in preclinical models?
Kartogenin demonstrates potential as a protective agent against doxorubicin-induced cardiotoxicity by alleviating oxidative stress and preserving mitochondrial function in preclinical models.
Hypothesis-generating for kartogenin in doxorubicin cardiotoxicity; clinical translation remains untested and should not change practice.
Doxorubicin (DOX) is a common antitumor drug in clinical practice, but its clinical use is limited due to its cardiotoxic side effects. Oxidative stress and mitochondrial damage are involved in DOX-induced cardiotoxicity (DIC). Kartogenin (KGN) has been shown to have a potent ability to resist oxidative stress and maintain mitochondrial homeostasis. But the impact of KGN on DIC has not been reported. This study explores the potential protective effect of KGN on DIC. The effect of KGN on DIC was studied by establishing in vivo and in vitro DIC models. KGN reduced DOX-induced cardiac insufficiency, myocardial injury, oxidative stress damage, and mitochondrial dysfunction. Through network pharmacology and RNA sequencing (RNA-seq), the mechanism of KGN anti-DIC was highly correlated with oxidative stress and mitochondria. These findings suggest that KGN is a valuable and promising strategy for the prevention of doxorubicin cardiotoxicity.
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Zhang et al. (2025) studied Doxorubicin-induced cardiotoxicity. Kartogenin (KGN) was evaluated on Cardiac insufficiency, myocardial injury, oxidative stress damage, and mitochondrial dysfunction. Kartogenin reduced doxorubicin-induced cardiac insufficiency, myocardial injury, oxidative stress damage, and mitochondrial dysfunction in in vivo and in vitro models.
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