Abstract
Left ventricular (LV) hypertrophy and associated heart failure are becoming a more prevalent and critical public health issue with the aging of society, and are exacerbated by reactive oxygen species (ROS). Dietary restriction (DR) markedly inhibits senescent changes; however, prolonged DR is difficult. We herein investigated whether preconditioning with short-term DR attenuates chronic pressure overload-induced cardiac hypertrophy and associated oxidative stress. Male c57BL6 mice were randomly divided into an ad libitum (AL) diet or 40% restricted diet (DR preconditioning, DRPC) group for 2 weeks prior to ascending aortic constriction (AAC), and all mice were fed ad libitum after AAC surgery. Two weeks after surgery, pressure overload by AAC increased LV wall thickness in association with LV diastolic dysfunction and promoted myocyte hypertrophy and cardiac fibrosis in the AL+AAC group. Oxidative stress in cardiac tissue and mitochondria also increased in the AL+AAC group in association with increments in cardiac NADPH oxidase-derived and mitochondrial ROS production. LV hypertrophy and associated cardiac dysfunction and oxidative stress were significantly attenuated in the DRPC+AAC group. Moreover, less severe mitochondrial oxidative damage in the DRPC+AAC group was associated with the suppression of mitochondrial permeability transition and cardiac apoptosis. These results indicate that chronic pressure overload-induced cardiac hypertrophy in association with cardiac and mitochondrial oxidative damage were attenuated by preconditioning with short-term DR.
Highlights
Dietary restriction (DR) is defined as a reduced caloric intake without malnutrition and is a powerful non-genomic intervention that has been shown to extend the life spans of experimental animals and prevent age-associated diseases, such as neurodegenerative diseases, cancer, and cardiovascular diseases in experimental animals and humans [1,2,3]
Extensive research on DR indicated that the mechanisms underlying its beneficial effects involve the suppression of insulin/insulin growth factor signaling, the target of rapamycin (TOR) pathway, reactive oxygen species (ROS) production, the promotion of the 5 adenosine monophosphate-activated protein kinase (AMPK), and sirtuin signaling pathways [2,11,12,13,14]
Consistent with the results obtained for the myocyte cross-sectional area, preconditioning with 2 weeks of DR did not affect myocardial Brain Natriuretic Peptide (BNP) mRNA expression levels before surgery (Figure 3d)
Summary
Dietary restriction (DR) is defined as a reduced caloric intake without malnutrition and is a powerful non-genomic intervention that has been shown to extend the life spans of experimental animals and prevent age-associated diseases, such as neurodegenerative diseases, cancer, and cardiovascular diseases in experimental animals and humans [1,2,3]. DR was found to prevent major risk factors for cardiovascular diseases, such as hypertension, dyslipidemia, and glucose intolerance, in experimental animals and humans [1,2,3,4]. It protected against aging- and diabetes-related cardiomyopathy [5,6], ischemic heart diseases [7], and cardiac hypertrophy [8,9] in animal models. The present study investigated the preconditioning effects of short-term DR on pressure overload-induced cardiac hypertrophy and associated oxidative stress in mice
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