Updating Experimental Models of Diabetic Cardiomyopathy

被引:61
作者
Fuentes-Antras, J. [1 ]
Picatoste, B. [1 ,2 ]
Gomez-Hernandez, A. [2 ,3 ]
Egido, J. [1 ,2 ]
Tunon, J. [1 ]
Lorenzo, O. [1 ,2 ]
机构
[1] Univ Autonoma Madrid, IIS Fdn Jimenez Diaz, Madrid 28040, Spain
[2] Spanish Biomed Res Ctr Diabet & Associated Metab, CIBERDEM, Madrid 28040, Spain
[3] Univ Complutense Madrid, Sch Pharm, Dept Biochem & Mol Biol, E-28040 Madrid, Spain
关键词
CARDIAC LIPID-ACCUMULATION; ISOLATED WORKING HEARTS; GLUCAGON-LIKE PEPTIDE-1; OXIDATIVE STRESS; DIASTOLIC DYSFUNCTION; MOUSE MODEL; CONTRACTILE DYSFUNCTION; INSULIN-RESISTANCE; MITOCHONDRIAL DYSFUNCTION; MYOCARDIAL HYPERTROPHY;
D O I
10.1155/2015/656795
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Diabetic cardiomyopathy entails a serious cardiac dysfunction induced by alterations in structure and contractility of the myocardium. This pathology is initiated by changes in energy substrates and occurs in the absence of atherothrombosis, hypertension, or other cardiomyopathies. Inflammation, hypertrophy, fibrosis, steatosis, and apoptosis in the myocardium have been studied in numerous diabetic experimental models in animals, mostly rodents. Type I and type II diabetes were induced by genetic manipulation, pancreatic toxins, and fat and sweet diets, and animals recapitulate the main features of human diabetes and related cardiomyopathy. In this review we update and discuss the main experimental models of diabetic cardiomyopathy, analysing the associated metabolic, structural, and functional abnormalities, and including current tools for detection of these responses. Also, novel experimental models based on genetic modifications of specific related genes have been discussed. The study of specific pathways or factors responsible for cardiac failures may be useful to design new pharmacological strategies for diabetic patients.
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页数:15
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