- •Short-term caloric restriction (CR) improves cardiac hypertrophy caused by pressure overload.
- •CR attenuates mitochondrial and NADPH oxidase–dependent ROS production.
- •CR preserves SOD and glutathione peroxidase activities in hypertrophic heart.
- •CR suppresses cardiac oxidative injury and improves diastolic function.
Caloric restriction (CR) prevents senescent changes, in which reactive oxygen species (ROS) have a critical role. Left ventricular (LV) hypertrophy is a risk factor for cardiovascular diseases. We examined whether CR alters cardiac redox state and hypertrophy from chronic pressure overload.
Methods and Results
Male c57BL6 mice were subjected to ascending aortic constriction (AAC) with ad libitum caloric intake (AL + AAC group) or 40% restricted caloric intake (CR + AAC group). CR was initiated 2 weeks before AAC and was continued for 4 weeks. Two weeks after constriction, AAC increased LV wall thickness, impaired transmitral flow velocity, and augmented myocyte hypertrophy and fibrosis, in association with enhancement of BNP and collagen III expressions in the AL + AAC group. In the AL + AAC group, oxidative stress in cardiac tissue and mitochondria were enhanced, and NADPH oxidase activity and mitochondrial ROS production were elevated. These changes were significantly attenuated in the CR + AAC group. Additionally, in antioxidant systems, myocardial glutathione peroxidase and superoxide dismutase activities were enhanced in the CR + AAC group.
Chronic pressure overload increased cardiac oxidative damage, in association with cardiac hypertrophy and fibrosis. Short-term CR suppressed oxidative stress and improved cardiac function, suggesting that short-term CR could be a useful strategy to prevent pressure overload–induced cardiac injury.
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Published online: May 13, 2015
Accepted: April 29, 2015
Received in revised form: March 30, 2015
Received: November 25, 2014
The first 2 authors contributed equally to this work.
Funding: Supported in part by “The Open Research Program” of Kyoto Pharmaceutical University from the Ministry of Education, Science, and Culture of Japan.
See page 665 for disclosure information.
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