Glucose-induced cell signaling in the pathogenesis of diabetic cardiomyopathy

被引:24
作者
Mortuza, Rokhsana [1 ]
Chakrabarti, Subrata [1 ]
机构
[1] Univ Western Ontario, Dept Pathol, London, ON N6A 5C1, Canada
基金
加拿大健康研究院;
关键词
Diabetic cardiomyopathy; Endothelial cell; Cardiomyocyte; Signaling; PROTEIN-KINASE-C; NF-KAPPA-B; ENDOTHELIUM-DEPENDENT VASODILATION; GLYCATION END-PRODUCTS; MAILLARD REACTION-PRODUCTS; MYOCYTE ENHANCER FACTOR-2; INDUCED OXIDATIVE STRESS; II HISTONE DEACETYLASES; SMOOTH-MUSCLE-CELLS; ALDOSE REDUCTASE;
D O I
10.1007/s10741-013-9381-z
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Chronic diabetic complications affect multiple organ systems and lead to significant morbidity and mortality in the diabetic population. Diabetic cardiomyopathy is a major etiologic factor causing heart failure. Dysfunction of both vascular endothelial cells and cardiomyocytes contributes in the pathogenesis of diabetic cardiomyopathy. Hyperglycemia has been identified as the key determinant in the development of several chronic diabetic complications. Hyperglycemia leads to oxidative stress and several other abnormalities causing changes in cellular signaling. These diabetes-mediated biochemical anomalies show cross-interaction and complex interplay. Such changes also cause alteration of transcriptional and post-transcriptional machinery causing altered production of vasoactive and cardioactive factors. In this review, we will highlight some of the important signaling changes leading to diabetic cardiomyopathy and discuss possible potential therapeutic remedies.
引用
收藏
页码:75 / 86
页数:12
相关论文
共 188 条
[1]   DIMINISHED ARTERIAL ELASTICITY IN DIABETES - ASSOCIATION WITH FLUORESCENT ADVANCED GLYCOSYLATION END-PRODUCTS IN COLLAGEN [J].
AIRAKSINEN, KEJ ;
SALMELA, PI ;
LINNALUOTO, MK ;
IKAHEIMO, MJ ;
AHOLA, K ;
RYHANEN, LJ .
CARDIOVASCULAR RESEARCH, 1993, 27 (06) :942-945
[2]  
*AM DIAB ASS, 1993, DIABETES CARE, V16, P72
[3]  
[Anonymous], AM J PHYSL
[4]   ACTIVATION OF CAMP AND MITOGEN RESPONSIVE GENES RELIES ON A COMMON NUCLEAR FACTOR [J].
ARIAS, J ;
ALBERTS, AS ;
BRINDLE, P ;
CLARET, FX ;
SMEAL, T ;
KARIN, M ;
FERAMISCO, J ;
MONTMINY, M .
NATURE, 1994, 370 (6486) :226-229
[5]   Cross-linking of glycated collagen in the pathogenesis of arterial and myocardial stiffening of aging and diabetes [J].
Aronson, D .
JOURNAL OF HYPERTENSION, 2003, 21 (01) :3-12
[6]   The SV40 large T antigen and adenovirus E1a oncoproteins interact with distinct isoforms of the transcriptional co-activator, p300 [J].
Avantaggiati, ML ;
Carbone, M ;
Graessmann, A ;
Nakatani, Y ;
Howard, B ;
Levine, AS .
EMBO JOURNAL, 1996, 15 (09) :2236-2248
[7]   NF-kappa B: Ten years after [J].
Baeuerle, PA ;
Baltimore, D .
CELL, 1996, 87 (01) :13-20
[8]   Cell cycle-dependent variations in c-Jun and JunB phosphorylation: a role in the control of cyclin D1 expression [J].
Bakiri, L ;
Lallemand, D ;
Bossy-Wetzel, E ;
Yaniv, M .
EMBO JOURNAL, 2000, 19 (09) :2056-2068
[9]   MicroRNAs: Genomics, biogenesis, mechanism, and function (Reprinted from Cell, vol 116, pg 281-297, 2004) [J].
Bartel, David P. .
CELL, 2007, 131 (04) :11-29
[10]   Role of oxidative stress in diabetic complications - A new perspective on an old paradigm [J].
Baynes, JW ;
Thorpe, SR .
DIABETES, 1999, 48 (01) :1-9