Institute of Cardiovascular Sciences, Department of Physiology, Faculty of Medicine, University of Manitoba, St. Boniface Hospital Research, 351 Tache Avenue, Winnipeg, MB, R2H 2A6, Canada.
Heart Fail Rev. 2014 Jan;19(1):25-33. doi: 10.1007/s10741-013-9378-7.
Although heart disease due to diabetes is mainly associated with complications of the large vessels, microvascular abnormalities are also considered to be involved in altering cardiac structure and function. Three major defects, such as endothelial dysfunction, alteration in the production/release of hormones, and shift in metabolism of smooth muscle cells, have been suggested to produce damage to the small arteries and capillaries (microangiopathy) due to hyperglycemia, and promote the development of diabetic cardiomyopathy. These factors may either act alone or in combination to produce oxidative stress as well as changes in cellular signaling and gene transcription, which in turn cause vasoconstriction and structural remodeling of the coronary vessels. Such alterations in microvasculature produce hypoperfusion of the myocardium and thereby lower the energy status resulting in changes in Ca(2+)-handling, apoptosis, and decreased cardiac contractile force. This article discusses diabetes-induced mechanisms of microvascular damage leading to cardiac dysfunction that is characterized by myocardial dilatation, cardiac hypertrophy as well as early diastolic and late systolic defects. Metabolic defects and changes in neurohumoral system due to diabetes, which promote disturbances in vascular homeostasis, are highlighted. In addition, increase in the vulnerability of the diabetic heart to the development of heart failure and the signaling pathways integrating nuclear factor κB and protein kinase C in diabetic cardiomyopathy are also described for comparison.
尽管糖尿病引起的心脏病主要与大血管并发症有关，但微血管异常也被认为参与了心脏结构和功能的改变。由于高血糖，三种主要的缺陷，如内皮功能障碍、激素产生/释放的改变以及平滑肌细胞代谢的转移，被认为会导致小动脉和毛细血管（微血管病变）受损，并促进糖尿病心肌病的发展。这些因素可能单独或联合作用产生氧化应激以及细胞信号转导和基因转录的变化，进而导致冠状动脉血管的收缩和结构重塑。微血管的这种改变导致心肌灌注不足，从而降低能量状态，导致 Ca(2+)-处理、细胞凋亡和心肌收缩力下降的变化。本文讨论了糖尿病引起的微血管损伤导致心脏功能障碍的机制，其特征是心肌扩张、心脏肥大以及早期舒张和晚期收缩缺陷。强调了由于糖尿病导致的代谢缺陷和神经激素系统的变化，促进了血管内稳态的紊乱。此外，还描述了糖尿病心脏对心力衰竭发展的易感性增加以及整合核因子 κB 和蛋白激酶 C 的信号通路，以便进行比较。
