4.6 Article

Apelin-13 impedes foam cell formation by activating Class III PI3K/Beclin-1-mediated autophagic pathway

期刊

出版社

ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.bbrc.2015.09.045

关键词

Apelin-13; Cholesterol efflux; Class III PI3K/Beclin-1; Autophagy; Macrophage foam cells

资金

  1. National Natural Sciences Foundation of China [81300224, 81370377, 81170278]
  2. construct program of the key discipline in Hunan province
  3. Zhengxiang Scholar Program of University of South China [2014-004]
  4. Science and Technology Project of Hunan Province [2014TT2018]
  5. Aid Program for Science and Technology Bureau of Hengyang City [2014KJ08]

向作者/读者索取更多资源

Apelin-13, an adipokine, promotes cholesterol efflux in macrophages with antiatherosclerotic effect. Autophagy, an evolutionarily ancient response to cellular stress, has been involved in atherosclerosis. Therefore, the purpose of this study was to investigate whether apelin-13 regulates macrophage foam cell cholesterol metabolism through autophagy, and also explore the underlying mechanisms. Here, we revealed that apelin-13 decreased lipid accumulation in THP-1 derived macrophages through markedly enhancing cholesterol efflux. Our study further demonstrated that apelin-13 induced autophagy via activation of Class III phosphoinositide 3-kinase (PI3K) and Beclin-1. Inhibition of Class III PI3K and Beclin-1 suppressed the stimulatory effects of apelin-13 on autophagy activity. The present study concluded that apelin-13 reduces lipid accumulation of foam cells by activating autophagy via Class III PI3K/Beclin-1 pathway. Therefore, our results provide brand new insight about apelin-13 inhibiting foam cell formation and highlight autophagy as a promising therapeutic target in atherosclerosis. (C) 2015 Elsevier Inc. All rights reserved.

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