ArticlePloS one2023
Cinnamaldehyde alleviates doxorubicin-induced cardiotoxicity by decreasing oxidative stress and ferroptosis in cardiomyocytes.
Article in PloS one, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 32 citations in OpenAlex.
- Research Progress on the Role of Traditional Chinese Medicine in Regulating Ferroptosis in Cardiovascular Diseases.Biology · 2026Review
- Doxorubicin-Induced Cardiac Remodeling: Mechanisms and Mitigation Strategies.Cardiovascular drugs and therapy · 2026Review
- Ferroptosis regulation in doxorubicin-induced cardiotoxicity: multi-mechanism interventions and translational strategies.Frontiers in pharmacology · 2026Review
- Sacubitril valsartan combined with bisoprolol reduces doxorubicin-induced cardiotoxicity in rats by attenuating oxidative stress.Experimental biology and medicine (Maywood, N.J.) · 2026Article
- Research progress on targeting autophagy pathways with medicinal plants and their active metabolites for the treatment of heart failure.Frontiers in pharmacology · 2026Review
- Growth differentiation factor 11 attenuates doxorubicin-induced cardiotoxicity by inhibiting myocardial pyroptosis and oxidative stress.Molecular and cellular biochemistry · 2026Article
- Cinnamaldehyde attenuates LPS-induced acute kidney injury by inhibiting ferroptosis via the Gsk3β/Nrf2/Gpx4 pathway.American journal of translational research · 2026Article
- Phytoconstituents-mediated Targeting of Ferroptosis for the Treatment of Cardiovascular Disease.Current cardiology reviews · 2026Review
- Essential Oils as Antioxidants: Mechanistic Insights from Radical Scavenging to Redox Signaling.Antioxidants (Basel, Switzerland) · 2025Review
- α-Bromocinnamaldehyde combats ESKAPE pathogens through dual bactericidal mechanism.Folia microbiologica · 2025Article
- Inetetamab triggers cardiotoxicity through its interaction with apoptosis, oxidative stress and autophagy pathways.Scientific reports · 2025Article
- Cinnamaldehyde supplementation in sows and their offspring: effects on colostrum and milk composition, performance, redox status and intestinal health.Journal of animal science and biotechnology · 2025Article
- Trillin protects against doxorubicin-induced cardiotoxicity through regulating Nrf2/HO-1 signaling pathway.PloS one · 2025Article
- Cardioprotective effect ofActa biochimica et biophysica Sinica · 2024Article
- Trace elements and metal nanoparticles: mechanistic approaches to mitigating chemotherapy-induced toxicity-a review of literature evidence.Biometals : an international journal on the role of metal ions in biology, biochemistry, and medicine · 2024Review
- Cinnamaldehyde: Pharmacokinetics, anticancer properties and therapeutic potential (Review).Molecular medicine reports · 2024Review
- Ferroptosis in organ fibrosis: From mechanisms to therapeutic medicines.Journal of translational internal medicine · 2024Article
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Although doxorubicin (DOX) is an efficient chemotherapeutic drug for human tumors, severe cardiotoxicity restricts its clinical use. Cinnamaldehyde (CA), a bioactive component isolated from Cinnamonum cassia, possesses potent anti-oxidative and anti-apoptotic potentials. The major aim of this study was to evaluate the protective role of CA against DOX-induced cardiotoxicity. To this end, cardiomyocyte injury models were developed using DOX-treated H9c2 cells and DOX-treated rats, respectively. Herein, we found that CA treatment increased cardiomyocyte viability and attenuated DOX-induced cardiomyocyte death in vitro. CA further protected rats against DOX-induced cardiotoxicity, as indicated by elevated creatine kinase (CK) and lactate dehydrogenase (LDH) levels, myocardium injury, and myocardial fibrosis. CA alleviated DOX-induced myocardial oxidative stress by regulating reactive oxygen species (ROS), malondialdehyde (MDA), superoxide dismutase (SOD), and glutathione (GSH) levels. Mechanistically, CA markedly accelerated nuclear translocation of nuclear erythroid factor 2-related factor 2 (Nrf2) and increased heme oxygenase-1 (HO-1) expression. Consequently, CA decreased DOX-induced cardiomyocyte ferroptosis, while Erastin (a ferroptosis agonist) treatment destroyed the effect of CA on increasing cardiomyocyte viability. Taken together, the current results demonstrate that CA alleviates DOX-induced cardiotoxicity, providing a promising opportunity to increase the clinical application of DOX.
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