Xiaoyan Dai
Guangzhou Medical University
38 Papers
124 Citations
Xiaoyan Dai is an academic researcher from Guangzhou Medical University. The author has contributed to research in topics: Chemistry & Inflammation. The author has an hindex of 16, co-authored 30 publications. Previous affiliations of Xiaoyan Dai include University of South China & University of Oklahoma Health Sciences Center.
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Papers
Phosphate-induced autophagy counteracts vascular calcification by reducing matrix vesicle release
Xiaoyan Dai,Ming-Ming Zhao,Yan Cai,Qing-Cong Guan,Ying Zhao,Youfei Guan,Wei Kong,Wei-Guo Zhu,Mingjiang Xu,Xian Wang +9 more
TL;DR: 3-methyladenine may be an endogenous protective mechanism counteracting phosphate-induced vascular calcification by reducing matrix vesicle release, andTherapeutic agents influencing the autophagic response may be of benefit to treat aging or disease-relatedascular calcification and osteoporosis.
213
Activation of AMPKα2 in adipocytes is essential for nicotine-induced insulin resistance in vivo.
Yue Wu,Ping Song,Wencheng Zhang,Junhui Liu,Xiaoyan Dai,Zhaoyu Liu,Qiulun Lu,Changhan Ouyang,Zhonglin Xie,Zhengxing Zhao,Xiaozhen Zhuo,Benoit Viollet,Marc Foretz,Jiliang Wu,Zuyi Yuan,Ming-Hui Zou +15 more
TL;DR: AMPKα2 is established as an essential mediator of nicotine-induced whole-body IR in spite of reductions in adiposity, and thereby causes IR in insulin-sensitive tissues.
153
The role of the LncRNA-FA2H-2-MLKL pathway in atherosclerosis by regulation of autophagy flux and inflammation through mTOR-dependent signaling.
Feng-Xia Guo,Qian Wu,Pan Li,Lei Zheng,Shu Ye,Xiaoyan Dai,Chun-Min Kang,Jing-Bo Lu,Bang-Ming Xu,Yuan-Jun Xu,Lei Xiao,Zhi-Feng Lu,Huan-Lan Bai,Yan-Wei Hu,Qian Wang +14 more
TL;DR: The findings indicated that the lnc RNA-FA2H-2-MLKL pathway is essential for regulation of autophagy and inflammation, and suggested that lncRNA-FA1H-1 and MLKL could act as potential therapeutic targets to ameliorate atherosclerosis-related diseases.
Macrophage Liver Kinase B1 Inhibits Foam Cell Formation and Atherosclerosis
TL;DR: It is concluded that macrophage LKB1 reduction caused by oxidized low-density lipoprotein promotes foam cell formation and the progression of atherosclerosis.
70
FUNDC1-dependent mitochondria-associated endoplasmic reticulum membranes are involved in angiogenesis and neoangiogenesis.
TL;DR: Zhang et al. as mentioned in this paper found that decreased MAMs formation by silencing FUNDC1 can inhibit angiogenesis by decreasing VEGFR2 expression and reducing tube formation, spheroid-sprouting and functional blood vessel formation in vitro and in vivo.