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AMPK的激活抑制肺动脉平滑肌细胞增殖。

Activation of AMPK inhibits pulmonary arterial smooth muscle cells proliferation.

作者信息

Wu Yuanyuan, Liu Lu, Zhang Yonghong, Wang Guizuo, Han Dong, Ke Rui, Li Shaojun, Feng Wei, Li Manxiang

机构信息

Department of Respiratory Medicine, Respiratory Diseases Research Center, The Second Affiliated Hospital of Medical College, Xi'an Jiaotong University, Xi'an, Shaanxi, PR China.

出版信息

Exp Lung Res. 2014 Jun;40(5):251-8. doi: 10.3109/01902148.2014.913092.

Abstract

The aims of the present study were to examine the effect of AMPK activation on pulmonary arterial smooth muscle cells (PASMCs) proliferation and to address its potential mechanisms. ET-1 dose and time-dependently induced PASMCs proliferation, and this effect was suppressed by a selective AMPK activator metformin. The results of the study further indicated that the proliferation of PASMCs stimulated by ET-1 was associated with the increase of Skp2 and decrease of p27, and metformin reversed ET-1-induced Skp2 elevation and raised p27 protein level. Our study suggests that activation of AMPK suppresses PASMCs proliferation and has potential value in negatively modulating pulmonary vascular remodeling and therefore could prevent or treat the development of pulmonary arterial hypertension (PAH).

摘要

本研究的目的是探讨AMPK激活对肺动脉平滑肌细胞(PASMCs)增殖的影响,并阐明其潜在机制。ET-1以剂量和时间依赖性方式诱导PASMCs增殖,而选择性AMPK激活剂二甲双胍可抑制这种作用。研究结果进一步表明,ET-1刺激的PASMCs增殖与Skp2增加和p27减少有关,二甲双胍可逆转ET-1诱导的Skp2升高并提高p27蛋白水平。我们的研究表明,AMPK激活可抑制PASMCs增殖,在负向调节肺血管重塑方面具有潜在价值,因此可能预防或治疗肺动脉高压(PAH)的发展。

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