ArticleInternational journal of molecular sciences2025
Kartogenin Improves Doxorubicin-Induced Cardiotoxicity by Alleviating Oxidative Stress and Protecting Mitochondria.
Article in International journal of molecular sciences, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
4 citing papers in PubMed.
- Celastrol Attenuates Doxorubicin-Induced Heart Failure by Preserving Mitochondrial Integrity and Suppressing Oxidative Stress and Is Accompanied by Changes in Gut Microbiota.Pharmaceuticals (Basel, Switzerland) · 2026Article
- Sacubitril valsartan combined with bisoprolol reduces doxorubicin-induced cardiotoxicity in rats by attenuating oxidative stress.Experimental biology and medicine (Maywood, N.J.) · 2026Article
- Exploring kartogenin: advances in therapeutics and signaling mechanisms for musculoskeletal regeneration.Molecular biology reports · 2025Review
- Doxorubicin-Induced Cardiotoxicity: A Comprehensive Update.Journal of cardiovascular development and disease · 2025Review
Corrections and comments
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Authors and funding
7 authors.
Funding
Abstract
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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Registered trials
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