Impact of conditioning hyperglycemic on myocardial infarction rats:Cardiac cell survival factors  

作　　者：Christiane Malfitano Alcione Lescano de Souza Junior Maria Cláudia Irigoyen 

机构地区：[1]Laboratório de Fisiologia Translacional,UNINOVE,01504001 S?o Paulo,Brazil [2]Universidade Nove de Julho-Medicine Program,01504001 S?o Paulo,Brazil [3]Instituto do Cora??o,Universidade de S?o Paulo,Faculdade de Medicina,05403900 S?o Paulo,Brazil [4]Nursing Department,University of Mato-Grosso,78200000 Mato Grosso,Brazil

出　　处：《World Journal of Cardiology》2014年第6期449-454,共6页世界心脏病学杂志（英文版）（电子版）

摘　　要：While clinical data have suggested that the diabetic heart is more susceptible to ischemic heart disease(IHD),animal data have so far pointed to a lower probability of IHD. Thus,the aim of this present review is to look at these conflicting results and discuss the protective mechanisms that conditioned hyperglycemia may confer to the heart against ischemic injury. Several mechanisms have been proposed to explain the cardioprotective action of high glucose exposure,namely,upregulation of anti-apoptotic factor Bcl-2,inactivation of pro-apoptotic factor bad,and activation of pro-survival factors such as protein kinase B(Akt),vascular endothelial growth factor(VEGF),hypoxia inducible factor-1α and protein kinase C-ε. Indeed,cytosolic increase in Ca2+ concentration,the mitochondrial permeability transition pore,plays a key role in the genesis of ischemic injury. Previous studies have shown that the diabetic heart decreased Na+/Ca2+ and Na+/H+ exchanger activity and as such it accumulates less Ca2+ in cardiomyocyte,thus preventing cardiac injury and the associated heart dysfunctions. In addition,the expression of VEGFin diabetic animals leads to increased capillary density before myocardial infarction. Despite poor prognostic in the long-term,all these results suggest that diabetes mellitus and consequently hyperglycemia may indeed play a cardioprotective role against myocardial infarction in the short term.While clinical data have suggested that the diabetic heart is more susceptible to ischemic heart disease(IHD),animal data have so far pointed to a lower probability of IHD. Thus,the aim of this present review is to look at these conflicting results and discuss the protective mechanisms that conditioned hyperglycemia may confer to the heart against ischemic injury. Several mechanisms have been proposed to explain the cardioprotective action of high glucose exposure,namely,upregulation of anti-apoptotic factor Bcl-2,inactivation of pro-apoptotic factor bad,and activation of pro-survival factors such as protein kinase B(Akt),vascular endothelial growth factor(VEGF),hypoxia inducible factor-1α and protein kinase C-ε. Indeed,cytosolic increase in Ca2+ concentration,the mitochondrial permeability transition pore,plays a key role in the genesis of ischemic injury. Previous studies have shown that the diabetic heart decreased Na+/Ca2+ and Na+/H+ exchanger activity and as such it accumulates less Ca2+ in cardiomyocyte,thus preventing cardiac injury and the associated heart dysfunctions. In addition,the expression of VEGFin diabetic animals leads to increased capillary density before myocardial infarction. Despite poor prognostic in the long-term,all these results suggest that diabetes mellitus and consequently hyperglycemia may indeed play a cardioprotective role against myocardial infarction in the short term.

关 键 词：Conditioned hyperglycemia Diabetes mellitus Myocardial infarction CARDIOPROTECTION Survival factors 

分 类 号：R542.22[医药卫生—心血管疾病]