High glucose/High Lipids impair vascular adiponectin function via inhibition of caveolin-1/AdipoR1 signalsome formation
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- 作者：Gai-Zhen Liua ; 1 ; Bin Lianga ; 1 ; Wayne Bond Laub ; Yang Wangb ; Jianli Zhaoc ; Rui Lid ; Xi Wangc ; Yuexing Yuanb ; Bernard L. Lopezb ; Theodore A. Christopherb ; Chuanshi Xiaoa ; Xin-Liang Mab ; xin.ma@jefferson.edu" class="auth_mail" title="E-mail the corresponding author ; Yajing Wangb ; d ; Yajing.Wang@jefferson.edu" class="auth_mail" title="E-mail the corresponding author
- 关键词：AdipoR1 ; Adiponectin receptor 1 ; AdipoR2 ; Adiponectin receptor 2 ; AMPK ; AMP activated protein kinase ; APN ; Adiponectin ; BFs ; Buoyant membrane fractions ; Cav1 ; Caveolin-1 ; CVD ; Cardiovascular disease ; eNOS ; Endothelial nitric oxide synthase ; HG/HL ; High glucose and high lipid ; HUVEC ; Human umbilical vein cells ; ICAM-1 ; Intercellular adhesion molecule-1 ; NO ; Nitric oxide
- 刊名：Free Radical Biology and Medicine
- 出版年：2015
- 出版时间：December 2015
- 年：2015
- 卷：89
- 期：Complete
- 页码：473-485
- 全文大小：2385 K
文摘
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The AdipoR1/Cav1 complex is critical for adiponectin signaling.
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Diabetes downregulated Cav1 expression and separated AdipoR1/Cav1 complex.
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Diabetes attenuates adiponectin's nitric oxide stimulatory and anti-oxidant actions.
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Adiponectin resistance contributes to diabetic endothelial dysfunction.