Pathological Anatomy and Clinical Morphology Department, Yerevan State Medical University after M. Heratsi, Yerevan, Republic of Armenia.
Director of Cardiology Research Institute of Tomsk National Research Medical Center of Russian Academy of Sciences, Tomsk, Russia.
Curr Probl Cardiol. 2022 Sep;47(9):101156. doi: 10.1016/j.cpcardiol.2022.101156. Epub 2022 Feb 19.
Diabetes mellitus (DM) provokes widely known structural and functional dyscoordination of the myocardium performance. A cascade of pathophysiological changes occurs due to metabolic disorders caused by hyperglycemia, insulin resistance, and dyslipidemia. Free fatty acids can stimulate oxidation and accumulate in the cytosol, leading to lipotoxic effects by forming ceramides, diacylglycerol, and reactive oxygen species (ROS). Hyperglycemia also causes an increase in the content of reactive oxygen species and the formation of advanced glycation end (AGE) products, which is accompanied by the development of cardiac glucotoxicity. The combination of these pathophysiological processes, ATP deficiency, and the development of myocardial fatty degeneration induce calcium stress, as well as dysfunction of mitochondria and endoplasmic reticulum, activation of signaling pathways of protein kinase C (PKC), mitogen-activated protein kinases (MAPK), etc., causing chronic sluggish inflammation, as well as first diastolic and further systolic dysfunction, and myocardial fibrosis. This article reviews the data on diabetic alteration of the cardiovascular system.
糖尿病（DM）引起心肌功能的广泛而熟知的结构和功能失调。由于高血糖、胰岛素抵抗和血脂异常引起的代谢紊乱，会引发一连串的病理生理变化。游离脂肪酸可以刺激氧化并在细胞质中积累，通过形成神经酰胺、二酰基甘油和活性氧物质（ROS）而导致脂毒性作用。高血糖还会导致活性氧物质含量增加和晚期糖基化终末产物（AGE）的形成，这伴随着心脏糖毒性的发展。这些病理生理过程、ATP 缺乏以及心肌脂肪变性的发展会导致钙应激，以及线粒体和内质网功能障碍、蛋白激酶 C（PKC）、丝裂原活化蛋白激酶（MAPK）等信号通路的激活，导致慢性迟钝性炎症，以及最初的舒张功能障碍和进一步的收缩功能障碍，以及心肌纤维化。本文综述了关于糖尿病对心血管系统影响的相关数据。
