Erucin Alleviates Cardiac Hypertrophy by Improving Mitochondrial Function via Nrf2‐Sirt3 Pathway

• DOI: 10.1002/ptr.8458
• Publication Date: 2025-05-26T07:56:02Z
• Authors: Shushu Jiang; Cheng Wang; Yin Dong; Long Chen; Menghao Shi; Fengxiao Zhang; Zhaohui Wang; Minglu Liang
• Keywords: SIRT3; Pressure overload; Phenylephrine; Ventricular remodeling

ABSTRACT Numerous studies have documented erucin's anticancer and vasodilatory properties, yet its impact on pathological cardiac hypertrophy remains to be fully understood. This study aimed explore the therapeutic potential of erucin in induced by pressure overload. Cardiac was mice transverse aortic constriction (TAC) surgery, neonatal rat cardiomyocytes via phenylephrine (PE) treatment. function remodeling were evaluated using echocardiography, histological assessment, molecular analyses. Mitochondrial assessed measuring mitochondrial respiration, ATP concentration, NAD+/NADH ratio, reactive oxygen species (ROS) levels. Molecular docking performed identify downstream effector. Nrf2 Sirt3 silenced siRNAs, their activities inhibited with ML385 3‐TYP, respectively. Here, we found that improved TAC‐induced hypertrophic mice, mitigated PE‐induced cell hypertrophy, restored function. analysis identified as a target protein erucin. Erucin increased levels activated signaling pathway, which turn promoted transcription. effect blocked silencing or ML385. Additionally, 3‐TYP abolished protective effects. is first demonstrate protects against improving through activation Nrf2‐Sirt3 pathway. may emerge promising candidate for treating hypertrophy.