Impaired hypoxia-inducible factor (HIF) regulation by hyperglycemia

被引:49
作者
Catrina, Sergiu-Bogdan [1 ,2 ]
机构
[1] Karolinska Univ Hosp, Rolf Luft Res Ctr Diabet & Endocrinol, Karolinska Inst, Dept Mol Med & Surg, S-17176 Stockholm, Sweden
[2] Karolinska Univ Hosp, Dept Endocrinol Metab & Diabet, S-17176 Stockholm, Sweden
来源
JOURNAL OF MOLECULAR MEDICINE-JMM | 2014年 / 92卷 / 10期
基金
瑞典研究理事会;
关键词
Hypoxia-inducible factor; Hyperglycaemia; Diabetes; Chronic complications; Pathogenic mechanisms; ENDOTHELIAL GROWTH-FACTOR; ALTERED GENE-EXPRESSION; GLYCATION END-PRODUCTS; PANCREATIC BETA-CELL; DIET-INDUCED OBESITY; DIABETIC MICE; FACTOR-I; MYOCARDIAL-INFARCTION; SKELETAL-MUSCLE; FACTOR; 1-ALPHA;
D O I
10.1007/s00109-014-1166-x
中图分类号
Q3 [遗传学];
学科分类号
071007 ; 090102 ;
摘要
The mechanisms that contribute to the development of diabetes complications remain unclear. A defective reaction of tissues to hypoxia has recently emerged as a new pathogenic mechanism and consists of a complex repression of hypoxia-inducible factor (HIF), which is the main regulator of the adaptive response to hypoxia. This paper discusses the mechanisms by which hyperglycaemia contributes to HIF repression in diabetes. Furthermore, a comprehensive analysis of the functional relevance of these new findings to the development of chronic diabetes complications is provided, along with examples from animal models and clinics.
引用
收藏
页码:1025 / 1034
页数:10
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