Key result
Eugenol mitigates cardiac hypertrophy by reducing ferroptosis and inflammation via 14-3-3γ/AMPKα2 signaling.
Why the study?
The mechanism by which eugenol attenuates cardiac hypertrophy related to ferroptosis, mitochondrial damage, and inflammation has not been fully elucidated.
Does eugenol pretreatment prevent cardiac hypertrophy, ferroptosis, and inflammation in preclinical models?
Does eugenol pretreatment prevent cardiac hypertrophy, ferroptosis, and inflammation in preclinical models?
Preclinical evidence indicates that eugenol mitigates cardiac hypertrophy by reducing ferroptosis and inflammation via the 14-3-3γ/AMPKα2 signaling pathway.
BACKGROUND: Chronic stress-induced cardiac hypertrophy is often accompanied by energy metabolism within the mitochondria, iron homeostasis, and inflammation. Eugenol (Eug), as an antioxidant, scavenges reactive oxygen species (ROS) in the body and stabilizes the internal cellular environment. However, the mechanism of this process has not been fully elucidated in existing studies. METHODS: In this experiment, hypertrophy of H9c2 cells was induced by angiotensin II (Ang Ⅱ), and cardiac hypertrophy was induced by transverse aortic constriction (TAC) in Sprague-Dawley (SD) rats. Subsequently, the impact of Eug pretreatment on cardiac hypertrophy, ferroptosis, mitochondrial injury, and inflammation along with the underlying molecular mechanisms, was investigated using an array of biomarkers. RESULTS: In vitro model, we demonstrated that both Eug and ferroptosis inhibitor (Ferrostatin-1, Fer-1) pretreatment decreased the expression of cardiac hypertrophy, cell surface area, and inflammatory specific biomarkers (IL6, TNFα), Malondialdehyde (MDA) content, ROS and Fe CONCLUSION: Our findings indicate that Eug reduces ferroptosis and inflammation, preserves mitochondrial function, and ultimately mitigates cardiac hypertrophy through the 14-3-3γ/AMPKα2 signaling pathway.
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Zhao et al. (2026) studied Cardiac hypertrophy. Eugenol vs. Control / Ferrostatin-1 was evaluated on Cardiac hypertrophy, ferroptosis, mitochondrial injury, and inflammation biomarkers. Eugenol pretreatment reduces ferroptosis and inflammation, preserves mitochondrial function, and mitigates cardiac hypertrophy through the 14-3-3γ/AMPKα2 signaling pathway.
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