Calorie Restriction Attenuates Monocrotaline-induced... : Journal of Cardiovascular Pharmacology (original) (raw)

Original Article

Calorie Restriction Attenuates Monocrotaline-induced Pulmonary Arterial Hypertension in Rats

Ding, Mingge MD, PhD†,‡; Lei, Jingyi MD*; Qu, Yinxian MD‡; Zhang, Huan MD*; Xin, Weichuan MD*; Ma, Feng MD*; Liu, Shuwen MD*; Li, Zhichao PhD§; Jin, Faguang MD†; Fu, Enqing MD, PhD†

*Department of Cardiology, Xi'an Central Hospital, Xi'an, China;

†Department of Respiratory Medicine, Tangdu Hospital, Fourth Military Medical University, Xi'an, China;

‡Department of Geriatrics, Xi'an Central Hospital, Xi'an, China; and

§Department of Pathophysiology, Fourth Military Medical University, Xi'an, China.

Reprints: Enqing Fu, MD, PhD, Department of Geriatrics, Xi'an Central Hospital, Xi'an 710038, China (e-mail: [email protected]).

Supported by grants from National Natural Science Foundation of China (No. 81270124).

The authors report no conflicts of interest.

M. Ding and J. Lei contributed equally to this study.

Received September 10, 2014

Accepted January 08, 2015

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Errata

Abstract

Calorie restriction (CR) is one of the most effective nonpharmacological interventions protecting against cardiovascular disease, such as hypertension in the systemic circulation. However, whether CR could attenuate pulmonary arterial hypertension (PAH) is largely unknown. The PAH model was developed by subjecting the rats to a single subcutaneous injection of monocrotaline. CR lowered mean pulmonary arterial pressure (mPAP) and reduced vascular remodeling and right ventricular hypertrophy in PAH rats. Meanwhile, CR attenuated endothelial dysfunction as evidenced by increased relaxation in response to acetylcholine. The beneficial effects of CR were associated with restored sirtuin-1 (SIRT1) expression and endothelial nitric oxide synthase (eNOS) phosphorylation and reduced eNOS acetylation in pulmonary arteries of PAH rats. To further clarify the role of SIRT1 in the protective effects of CR, adenoviral vectors for overexpression of SIRT1 were administered intratracheally at 1 day before monocrotaline injection. Overexpression of SIRT1 exhibited similar beneficial effects on mPAP and endothelial function, and increased eNOS phosphorylation and reduced eNOS acetylation in the absence of CR. Moreover, SIRT1 overexpression attenuated the increase in mPAP in hypoxia-induced PAH animals. Overall, the present data demonstrate that CR may serve as an effective treatment of PAH, and targeting the SIRT1/eNOS pathway may improve treatment of PAH.

Errata

In the article that appeared on page 562 of the June 2015 issue, the affiliations for the first author, Mingge Ding, were listed in the incorrect order. The affiliations in the correct order are:

[1Department of Geriatrics, Xi’an Central Hospital, Xi’an 710000, China; 2Department of Respiratory Medicine, Tangdu Hospital, Fourth Military Medical University, Xi’an 710038, China]

Journal of Cardiovascular Pharmacology. 66(5):514, November 2015.

In the article that appeared on page 562 of the June 2015 issue, the address given for the corresponding author, Enqing Fu, MD, PhD, was incorrect. The correct address is Department of Respiratory Medicine, Tangdu Hospital, Fourth Military Medical University.

Journal of Cardiovascular Pharmacology. 66(3):322, September 2015.