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Activation of catalase by apelin prevents oxidative stress‐linked cardiac hypertrophy
Author(s) -
Foussal Camille,
Lairez Olivier,
Calise Denis,
Pathak Atul,
Guilbeau-Frugier Celine,
Valet Philippe,
Parini Angelo,
Kunduzova Oksana
Publication year - 2010
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/j.febslet.2010.04.025
Subject(s) - apelin , oxidative stress , catalase , medicine , endocrinology , reactive oxygen species , muscle hypertrophy , chemistry , pressure overload , adipose tissue , oxidative phosphorylation , activator (genetics) , biology , cardiac hypertrophy , biochemistry , receptor
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.