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Honokiol Inhibits Arsenic Trioxide-Induced Cardiomyopathy by Modulating Ferroptosis via SIRT3 Signaling Pathway
Qing-Qing Wei1,2, An-Liang Huang2, Ning-Yi Liu1,2
1School of Basic Medicine, North Sichuan Medical College, Nanchong, Sichuan, China, scu.edu.cn.
Cardiology Research and Practice
|August 4, 2026
Summary
Honokiol (HKL) protects the heart from arsenic trioxide (ATO) damage by preventing ferroptosis, a cell death pathway. This protection is dependent on the SIRT3 signaling pathway and involves restoring autophagy.
Area of Science:
- Cardiovascular Biology
- Toxicology
- Cell Death Mechanisms
Background:
- Ferroptosis is a key mechanism in arsenic trioxide (ATO)-induced cardiotoxicity.
- Understanding protective strategies against ATO cardiotoxicity is crucial.
Purpose of the Study:
- To investigate if Honokiol (HKL) protects against ATO-induced cardiac injury by inhibiting ferroptosis.
- To elucidate the role of the SIRT3 signaling pathway in HKL's cardioprotective effects.
Main Methods:
- Utilized 129S1/SvImJ wild-type (WT) and SIRT3-knockout (SIRT3-/-) mice.
- Assessed myocardial injury, hypertrophy, oxidative stress markers (ROS, SOD2 acetylation, ATP), ferroptosis markers (iron, MDA, 4-HNE, GPX4, GSH), and autophagic flux.
- Investigated the impact of pharmacological or genetic inhibition of SIRT3 and autophagic flux.
Main Results:
- HKL attenuated ATO-induced myocardial injury and hypertrophy in a SIRT3-dependent manner.
- HKL reduced oxidative stress via the SIRT3/SOD2 pathway and inhibited ferroptosis.
- HKL restored ATO-impaired autophagic flux, which correlated with its protective effects.
Conclusions:
- HKL exhibits cardioprotective effects against ATO-induced cardiotoxicity.
- The protective mechanism involves inhibiting ferroptosis and restoring autophagic flux through the SIRT3 signaling pathway.
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