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Updated: Dec 27, 2025
Technique of Minimally Invasive Transverse Aortic Constriction in Mice for Induction of Left Ventricular Hypertrophy
Published on: September 25, 2017
A machine learning-driven study indicates emodin improves cardiac hypertrophy by modulation of mitochondrial SIRT3
Jian Gao1, Kunlin Zhang2, Yi Wang3
1Beijing University of Chinese Medicine, Beijing, 100029, China; The Third Affiliated Hospital, Beijing University of Chinese Medicine, Beijing, 100029, China.
Insights
Emodin, a component of rhubarb, effectively treats cardiac hypertrophy by protecting mitochondria. It activates SIRT3 signaling, offering a new therapeutic strategy for heart conditions.
Area of Science:
- Cardiovascular Research
- Pharmacology
- Mitochondrial Biology
Background:
- Cardiac hypertrophy (CH) significantly increases heart failure risk, lacking effective treatments.
- Mitochondrial protection is a promising strategy to combat CH.
- Rheum palmatum L. (rhubarb) shows potential in treating heart failure and inhibiting cardiac enlargement.
Purpose of the Study:
- To identify rhubarb's active components and molecular targets for treating CH.
- To elucidate the pharmacological mechanisms of rhubarb in CH treatment.
- To validate emodin's therapeutic potential and its underlying pathways in CH.
Main Methods:
- Network pharmacology and machine learning identified emodin-SIRT3 as a key interaction.
- Surflex docking confirmed emodin-SIRT3 as an optimal combination.
- In vivo (TAC/isoproterenol-induced CH mice) and in vitro (phenylephrine-injured cardiomyocytes) models were used.
Main Results:
- Emodin effectively inhibited agonist-induced and pressure overload-mediated CH.
- Emodin prevented mitochondrial dysfunction by activating SIRT3 signaling.
- PGC-1ɑ was identified as an upstream regulator in the emodin-SIRT3 pathway.
Conclusions:
- Emodin is a key pharmacodynamic component of rhubarb for treating CH.
- Emodin exerts therapeutic effects via mitochondrial protection through SIRT3 activation.
- This study clarifies rhubarb's mechanism and highlights emodin's potential for CH treatment.
Abstract:
Cardiac hypertrophy (CH) is an enormous risk factor in the process of heart failure development, however, there is still lack of effective treatment for CH. Mitochondrial protection is an effective way against CH. Rheum palmatum L. (rhubarb) has been used to treat chronic heart diseases such as heart failure, especially to inhibit cardiac compensatory enlargement. The aim of this study was to explore the pharmacodynamic component of rhubarb and reveal its pharmacological effects and targets in the treatment of CH. Based on network pharmacology and machine learning approach, ingredients of rhubarb and targets for CH were extracted and surflex docking was conducted for obtaining the optimal ingredient-target combination(s) and emodin-SIRT3 was identified for further functional analysis. Transverse aortic constriction or isoproterenol induced CH mice and phenylephrine injured cardiomyocytes were used to verify the mitochondria protection effect and CH improvement of emodin in vivo and in vitro by modulation of mitochondrial SIRT3 signaling. The results showed that emodin could block agonist-induced and pressure overload-mediated CH. Emodin prevented mitochondrial dysfunction and its underlying mechanism was attributed to the activation of SIRT3, but the effect was not obvious with the presence of SIRT3 inhibitors (3-TYP)/SIRT3 siRNA. Furthermore, PGC-1ɑ was involved in the process of emodin regulating SIRT3 signaling pathway as an upstream target. Our findings clarified the main material basis and mechanism of rhubarb in the treatment of CH. Emodin, as the major ingredient of rhubarb, has therapeutic potential for CH through mitochondrial protection due to the modulation of SIRT3 signaling.
