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Activation of catalase by apelin prevents oxidative stress-linked cardiac hypertrophy
Camille Foussal1, Olivier Lairez, Denis Calise
1Institut National de la Santé et de la Recherche Médicale (INSERM), U858, Toulouse, France.
Abstract:
Adipose tissue secretes a variety of bioactive factors, which can regulate cardiomyocyte hypertrophy via reactive oxygen species (ROS). In the present study we investigated whether apelin affects ROS-dependent cardiac hypertrophy. In cardiomyocytes apelin inhibited the hypertrophic response to 5-HT and oxidative stress induced by 5-HT- or H(2)O(2) in a dose-dependent manner. These effects were concomitant to the increase in mRNA expression and activity of catalase. Chronic treatment of mice with apelin attenuated pressure-overload-induced left ventricular hypertrophy. The prevention of hypertrophy by apelin was associated with increased myocardial catalase activity and decreased plasma lipid hydroperoxide, as an index of oxidative stress. These results show that apelin behaves as a catalase activator and prevents cardiac ROS-dependent hypertrophy.
Insights
Apelin, a bioactive factor, prevents cardiac hypertrophy by activating catalase and reducing oxidative stress. This finding offers new insights into managing heart conditions related to reactive oxygen species (ROS).
Area of Science:
- Cardiology
- Endocrinology
- Biochemistry
Background:
- Adipose tissue secretes factors influencing cardiomyocyte hypertrophy via reactive oxygen species (ROS).
- Understanding the role of specific factors like apelin in regulating cardiac hypertrophy is crucial.
Purpose of the Study:
- To investigate the effect of apelin on ROS-dependent cardiac hypertrophy.
- To determine if apelin modulates catalase activity and oxidative stress markers.
Main Methods:
- In vitro studies using cardiomyocytes exposed to 5-HT or H(2)O(2).
- In vivo studies involving chronic apelin treatment in mice subjected to pressure overload.
- Analysis of catalase mRNA expression, activity, and oxidative stress markers (lipid hydroperoxide).
Main Results:
- Apelin dose-dependently inhibited 5-HT- and H(2)O(2)-induced cardiomyocyte hypertrophy.
- Apelin treatment increased catalase mRNA expression and activity in cardiomyocytes.
- Chronic apelin administration in mice attenuated pressure-overload-induced cardiac hypertrophy, associated with increased myocardial catalase and decreased plasma lipid hydroperoxide.
Conclusions:
- Apelin acts as a catalase activator.
- Apelin effectively prevents cardiac hypertrophy mediated by reactive oxygen species (ROS).
- Apelin holds potential as a therapeutic agent for cardiac hypertrophy.
