Aleksandrovski Y A
Kantor Forschungsgruppe, Baden-Baden, 76499, Germany. Yakov.
Biochemistry (Mosc). 1998 Nov;63(11):1249-57.
The main molecular process responsible for the development of diabetic complications is the activation of intracellular protein kinase C by long-term hyperglycemia. In ordinary somatic cells (e.g., endothelial or retinal cells) this activation disturbs the metabolism of these cells, whereas a transition into an "excited state" of effector cells such as monocytes or polymorphonuclear leukocytes causes an avalanche-like increase of various pathological processes damaging the body. In relatively compensated diabetes mellitus, when the duration of hyperglycemia is not long and levels of hyperglycemia are not too high, the intensity of the above-mentioned processes is low. However, due to the long time course of reparative processes, some damages which appear in short periods of decompensation can accumulate in the body, finally causing the clinical manifestation of vascular complications of diabetes mellitus.
导致糖尿病并发症发生的主要分子过程是长期高血糖激活细胞内蛋白激酶C。在普通体细胞（如内皮细胞或视网膜细胞）中，这种激活会扰乱这些细胞的代谢，而效应细胞（如单核细胞或多形核白细胞）转变为“兴奋状态”会导致损害身体的各种病理过程呈雪崩式增加。在相对代偿性糖尿病中，当高血糖持续时间不长且血糖水平不太高时，上述过程的强度较低。然而，由于修复过程的时间较长，在短期失代偿期出现的一些损伤会在体内积累，最终导致糖尿病血管并发症的临床表现。
