Fibroblast growth factor 21 deletion aggravates diabetes-induced pathogenic changes in the aorta in type 1 diabetic mice

Cardiovascular Diabetology

Volumn 14, Issue 1, 2015, Pages

  Yan, Xiaoqing ^a,b,c   Chen, Jun ^a,c   Zhang, Chi ^a,b   Zeng, Jun ^c   Zhou, Shanshan ^c,d   Zhang, Zhiguo ^c,d   Lu, Xuemian ^b   Chen, Jing ^c   Feng, Wenke ^c   Li, Xiaokun ^a   Tan, Yi ^a,c  

^a WENZHOU MEDICAL UNIVERSITY   (China)

^b THE THIRD AFFILIATED HOSPITAL OF WENZHOU MEDICAL UNIVERSITY   (China)

^c University of Louisville School of Medicine   (United States)

^d THE FIRST HOSPITAL OF JILIN UNIVERSITY   (China)

Author keywords

Diabetes; Fibroblast growth factor 21; Oxidative stress; Vascular damage

Indexed keywords

3 NITROTYROCINE; 4 HYDROXYNONENAL; CHEMICAL COMPOUND; CONNECTIVE TISSUE GROWTH FACTOR; ENDOTHELIAL NITRIC OXIDE SYNTHASE; FIBROBLAST GROWTH FACTOR 21; TRANSFORMING GROWTH FACTOR BETA; TUMOR NECROSIS FACTOR ALPHA; UNCLASSIFIED DRUG; 3-NITROTYROSINE; 4-HYDROXY-2-NONENAL; ALDEHYDE; COLLAGEN; CTGF PROTEIN, MOUSE; FIBROBLAST GROWTH FACTOR; NOS3 PROTEIN, MOUSE; TUMOR NECROSIS FACTOR; TYROSINE;

ANIMAL CELL; ANIMAL EXPERIMENT; ANIMAL MODEL; ANIMAL TISSUE; AORTA DISEASE; AORTIC FIBROSIS; AORTIC INFLAMMATION; AORTIC REMODELING; APOPTOSIS; ARTICLE; BIOACCUMULATION; CELL DEATH; CONTROLLED STUDY; DISEASE EXACERBATION; ENZYME ACTIVATION; FGF21 GENE; GENE DELETION; INSULIN DEPENDENT DIABETES MELLITUS; MALE; MOUSE; NONHUMAN; OXIDATIVE STRESS; PATHOGENESIS; PROTEIN EXPRESSION; UPREGULATION; VASCULAR DISEASE; ANALOGS AND DERIVATIVES; ANIMAL; AORTA; AORTIC DISEASE; C57BL MOUSE; COMPLICATION; DEFICIENCY; DIABETIC ANGIOPATHY; EXPERIMENTAL DIABETES MELLITUS; FIBROSIS; GENETIC PREDISPOSITION; GENETICS; KNOCKOUT MOUSE; METABOLISM; PATHOLOGY; PHENOTYPE; SIGNAL TRANSDUCTION; TIME FACTOR; VASCULAR REMODELING;

ALDEHYDES; ANIMALS; AORTA; AORTIC DISEASES; APOPTOSIS; COLLAGEN; CONNECTIVE TISSUE GROWTH FACTOR; DIABETES MELLITUS, EXPERIMENTAL; DIABETES MELLITUS, TYPE 1; DIABETIC ANGIOPATHIES; FIBROBLAST GROWTH FACTORS; FIBROSIS; GENE DELETION; GENETIC PREDISPOSITION TO DISEASE; MALE; MICE, INBRED C57BL; MICE, KNOCKOUT; NITRIC OXIDE SYNTHASE TYPE III; OXIDATIVE STRESS; PHENOTYPE; SIGNAL TRANSDUCTION; TIME FACTORS; TRANSFORMING GROWTH FACTOR BETA; TUMOR NECROSIS FACTOR-ALPHA; TYROSINE; VASCULAR REMODELING;

EID: 84933520546     PISSN: None     EISSN: 14752840     Source Type: Journal    
DOI: 10.1186/s12933-015-0241-0     Document Type: Article

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