Highlights
- •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.
Abstract
Background
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.
Conclusions
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.
Key Words
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Article info
Publication history
Published online: May 13, 2015
Accepted:
April 29,
2015
Received in revised form:
March 30,
2015
Received:
November 25,
2014
Footnotes
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.
Identification
Copyright
© 2015 Elsevier Inc. Published by Elsevier Inc. All rights reserved.
