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12篇 您的检索式:作者名="Youfei Guan"
    题名 作者 年代 出处 被引量
1Peroxisome proliferator-activated receptors (PPARs): novel therapeutic targets in renal disease显示文摘GUAN Youfei BREYER M D 2001Kidney International2001,60,1:1
2Regulation of gastric hormones by systemic rapamycin显示文摘Geyang Xu Yin Li Wenjiao An Jing Zhao Xinxin Xiang Li Ding Ziru Li Youfei Guan Xian Wang Chaoshu Tang Yi Zhu Nanping Wang Xiaoying Li Michael Mulholland Weizhen Zhang 2010Peptides2010,,12:1
3Expression of peroxisome proliferator-activated receptors in urinary tract of rabbits and humans显示文摘Youfei Guan Yahua Zhang Linda Davis 1997Am J Physiol Renal Physiol1997,273,:1
4Thiazolidinediones expand body fluid volume through PPARγstimulation of EnaC-mediated renal salt absorption显示文摘 Chuanming Hao Dae Ryong Cha 2005Nature Medicine2005,11,:1
5Enhanced expression of cyclooxygenase-2 in high grade human transitional cell bladder carcinomas显示文摘Martin Kmhoff Youfei Guan Heidi W 2000Am J Path2000,157,7:1
6Peroxisome Proliferator-Activated Receptor Family and Its Relationship to Renal Complications of the Metabolic Syndrome显示文摘YOUFEI GUAN 0,,:1
7The mechanisms linking adiposopathy to type 2 diabetes显示文摘Obesity is defined as excessive accumulation of body fat in proportion to body size.When obesity occurs,the functions of adipose tissue may be deregulated,which is termed as adiposopathy.Adiposopathy is an independent risk factor for many diseases,including diabetes and cardiovascular diseases.In overweight or obese subjects with adiposopathy,hyperlipidemia exerts lipotoxicity in pancreatic islet and liver and induces pancreaticβcell dysfunction and liver insulin resistance,which are the decisive factors causing type 2 diabetes.Moreover,adipokines have been shown to play important roles in the regulation of glucose homeostasis.When adiposopathy occurs,abnormal changes in the serum adipokine profile correlate with the development and progression of pancreaticβcell dysfunction and insulin resistance in peripheral tissue.The current paper briefly discusses the latest findings regarding the effects of adiposopathy-related lipotoxicity and cytokine toxicity on the development of type 2 diabetes.Jichun Yang Jihong Kang Youfei Guan 2013Frontiers of Medicine2013,7,4:1
8Thiazolidinediones expand body fluid volume through PPAR γ stimulation of EnaC-mediated renal salt absorption显示文摘YouFei Guan Chuanming Hao Dae Ryong Cha 2005Nature medicine2005,11,8:1
9PPARγ as a therapeutic target in diabetic nephropathy and other renal diseases显示文摘Jichun Yang Yunfeng Zhou Youfei Guan 2012Current Opinion in Nephrology and Hypertension2012,,1:1
10Melatonin decreases GSDME mediated mesothelial cell pyroptosis and prevents peritoneal fibrosis and ultrafiltration failure显示文摘Peritoneal fibrosis together with increased capillaries is the primary cause of peritoneal dialysis failure.Mesothelial cell loss is an initiating event for peritoneal fibrosis.We find that the elevated glucose concentrations in peritoneal dialysate drive mesothelial cell pyroptosis in a manner dependent on caspase-3 and Gasdermin E,driving downstream inflammatory responses,including the activation of macrophages.Moreover,pyroptosis is associated with elevated vascular endothelial growth factor A and C,two key factors in vascular angiogenesis and lymphatic vessel formation.GSDME deficiency mice are protected from high glucose induced peritoneal fibrosis and ultrafiltration failure.Application of melatonin abrogates mesothelial cell pyroptosis through a MT1R-mediated action,and successfully reduces peritoneal fibrosis and angiogenesis in an animal model while preserving dialysis efficacy.Mechanistically,melatonin treatment maintains mitochondrial integrity in mesothelial cells,meanwhile activating m TOR signaling through an increase in the glycolysis product dihydroxyacetone phosphate.These effects together with quenching free radicals by melatonin help mesothelial cells maintain a relatively stable internal environment in the face of high-glucose stress.Thus,Melatonin treatment holds some promise in preserving mesothelium integrity and in decreasing angiogenesis to protect peritoneum function in patients undergoing peritoneal dialysis.Hongxia Ruan Xuejuan Li Lina Zhou Zihan Zheng Rulin Hua Xu Wang Yuan Wang Yujie Fan Shuwen Guo Lihua Wang Shafiq ur Rahman Ziwei Wang Yuyuan Wei Shuangyan Yu Rongzhi Zhang Qian Cheng Jie Sheng Xue Li Xiaoyan Liu Ruqiang Yuan Xiaoyan Zhang Lihong Chen Guowang Xu Youfei Guan Jing Nie Hongqiang Qin Feng Zheng 2024Science China(Life Sciences)2024,67,2:0
11Liver HMGCS2 is critical in the maintenance of liver lipid homeostasis during fasting显示文摘Fasting induces mammalian metabolic switch from glucose to fatty acid-derived ketones,resulting in a marked change in blood glucose,triglyceride,free fatty acid andβ-hydroxybutyrate levels and a phenotype of transient hepatic steatosis.However,the underlying mechanism remains incompletely understood.Yunfeng Zhou Tingting Gu Shuyuan Hu Zhaokang Luo Ling Huang Cong Yu Jie Wang Baohua Liu Xiaoyan Zhang Youfei Guan 2023Genes & Diseases2023,10,3:0
12MHC class Ⅱ in renal tubules plays an essential role in renal fibrosis显示文摘Immunomodulation has been considered a potential therapeutic approach for chronic kidney disease(CKD).Although it has been previously reported that CD4+T cells contribute to the development of renal fibrosis after UUO,the role of MHC class Ⅱ(MHCII)in UUO-induced renal fibrosis remains largely uncharacterized.The present study reports that the expressions of MHCII molecules in renal cortical tubules are upregulated in a mouse unilateral ureter obstruction(UUO)model.Global or renal tubule-specific ablation of MHCII significantly alleviates renal fibrosis following UUO.Additionally,renal expression of profibrotic genes showcased consistent reduction in both MHCII gene deficient mouse lines.These results demonstrate that renal tubular MHCII plays an important role in pathogenesis of renal fibrosis.Yunfeng Zhou Zhaokang Luo Chenghui Liao Rong Cao Zain Hussain Jie Wang Yeting Zhou Tie Chen Jie Sun Zhong Huang Baohua Liu Xiaoyan Zhang Youfei Guan Tuo Deng 2021Cellular & Molecular Immunology2021,18,11:0
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