Abstract
Heart failure is a frequent unfavorable outcome of pathological cardiac hypertrophy. Recent increase in dietary fructose consumption mirrors the rise in prevalence of cardiovascular diseases such as cardiac hypertrophy leading to concerns raised by public health experts. Mitochondria, comprising 30% of cardiomyocyte volume, play a central role in modulating redox-dependent cellular processes such as metabolism and apoptosis. Furthermore, mitochondrial dysfunction is a key cause of pathogenesis of fructose-induced cardiac hypertrophy. Naringin, a major flavanone glycoside in citrus species, has displayed strong antioxidant potential in models of oxidative stress. In this study, we evaluated protective effects of naringin against fructose-induced cardiac hypertrophy and associated mechanisms of action, using in vitro and in vivo models. We found that naringin suppressed mitochondrial ROS production and mitochondrial dysfunction in cardiomyocytes exposed to fructose and consequently reduced cardiomyocyte hypertrophy by regulating AMPK-mTOR signaling axis. Furthermore, naringin counteracted fructose-induced cardiomyocyte apoptosis, and this function of naringin was linked to its ability to inhibit ROS-dependent ATM-mediated p53 signaling. This result was supported by observations in in vivo mouse model of cardiac hypertrophy. These findings indicate a novel role for naringin in protecting against fructose-induced cardiac hypertrophy and suggest unique therapeutic strategies for prevention of cardiovascular diseases.
Highlights
Energy supply in the form of ATP is mandatory for sustaining cardiac contractile and relaxation functions
The aim was to determine whether naringin protected cardiomyocytes against ROS-mediated apoptosis and hypertrophy by modulating fructose-induced mitochondrial dysfunction to prevent cardiac injury, representing a novel protective approach for pathological cardiac hypertrophy resulting from dietary fructose consumption
The results indicated that the cardiomyocyte cell size was markedly increased after fructose treatment, whereas the addition of naringin led to a decrease in the fructose-induced enlargement of the cardiomyocytes (Fig. 1b)
Summary
Heart failure is a frequent unfavorable outcome of pathological cardiac hypertrophy. Recent increase in dietary fructose consumption mirrors the rise in prevalence of cardiovascular diseases such as cardiac hypertrophy leading to concerns raised by public health experts. Naringin counteracted fructose-induced cardiomyocyte apoptosis, and this function of naringin was linked to its ability to inhibit ROS-dependent ATM-mediated p53 signaling This result was supported by observations in in vivo mouse model of cardiac hypertrophy. Suggests that mitochondria play a very important role in the development of cardiac hypertrophy In both human subjects and experimental models of cardiac hypertrophy, mitochondrial dysfunction is increased[10,11,12]. The aim was to determine whether naringin protected cardiomyocytes against ROS-mediated apoptosis and hypertrophy by modulating fructose-induced mitochondrial dysfunction to prevent cardiac injury, representing a novel protective approach for pathological cardiac hypertrophy resulting from dietary fructose consumption
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