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. 2015 Dec;38(12):813-20.
doi: 10.1038/hr.2015.85. Epub 2015 Jul 30.

Augmentation of autophagy by atorvastatin via Akt/mTOR pathway in spontaneously hypertensive rats

Wei Wang  1   2 , Hao Wang  3 , Qing-Xin Geng  4 , Hua-Ting Wang  4 , Wei Miao  4 , Bo Cheng  2 , Di Zhao  5 , Guang-Min Song  1 , Groban Leanne  3 , Zhuo Zhao  4
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Augmentation of autophagy by atorvastatin via Akt/mTOR pathway in spontaneously hypertensive rats

Wei Wang et al. Hypertens Res. 2015 Dec.

Abstract

Autophagy is activated in hypertension-induced cardiac hypertrophy. However, the mechanisms and significance of an activated autophagy are not clear. This study was designed to determine the role of atorvastatin (ATO) in cardiac autophagy and associated benefits on cardiac remodeling and left ventricular function in spontaneously hypertensive rats (SHRs). Twenty-eight male SHRs at 8 weeks of age were randomized to treatment with vehicle (saline solution; SHR+V) or ATO (SHR+ATO; 50 mg kg(-1) per day) for 6 or 12 months. Age-matched male Wistar-Kyoto (WKY) rats were used as normotensive controls. Cardiac magnetic resonance was used to evaluate cardiac function and structure. Compared with WKY rats, SHRs showed significant left ventricle (LV) dysfunction, remodeling and increases in cardiomyocyte size, which were all attenuated by 6 and 12 months of ATO treatment. Compared with WKY rats, autophagy was activated in the hearts of SHRs and this effect was amplified by chronic ATO treatment, particularly following 12 months of treatment. Protein expression levels of microtubule-associated protein-1 light chain 3-II and beclin-1, the biomarkers of an activated cardiac autophagy, were significantly elevated in ATO-treated versus vehicle-treated SHRs and control WKY rats. Cardiac Akt and phosphorylated mammalian target of rapamycin (mTOR) expression were also increased in the hearts of SHR versus WKY rats, and this effect was attenuated by ATO treatment. These findings suggest that ATO-mediated improvements in LV function and structure in SHRs may be, in part, through its regulation of cardiac autophagy via the Akt/mTOR pathway.

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