Iwaki T, Hamada Y, Tateishi J
Department of Neuropathology, Faculty of Medicine, Kyushu University, Fukuoka, Japan.
Pathol Int. 1996 Oct;46(10):757-63. doi: 10.1111/j.1440-1827.1996.tb03545.x.
Using monospecific antibody for the advanced glycosylation end-products (AGEP), it was revealed that the AGEP localized in the basophilic degeneration of the myocardium and the corpora amylacea of the glia. The stability of the proteins that constitute those degenerative deposits suggests that they would be ideal substrates for non-enzymatic glycation, a process that occurs over a long time under a high glucose content, and ultimately results in the formation of the AGEP. Such deposits also exhibited evidence of stress reactions: the accumulation of HSP72, heme oxygenase-1 and ubiquitin. As recent studies have shown that AGEP-modified proteins aggregate and that they generate reactive oxygen intermediates, the accumulation of such heat shock proteins may reflect the oxidative stress concomitant with AGEP accumulation, and thereby promote their cellular dysfunction. Hereby, it is proposed that the age-related increase in the AGEP, that is, a fundamental aging process, is involved in the formation of the basophilic degeneration in the myocardium and the corpora amylacea of the glia.
使用针对晚期糖基化终产物（AGEP）的单特异性抗体，发现AGEP定位于心肌的嗜碱性变性和神经胶质细胞的淀粉样体中。构成这些退行性沉积物的蛋白质的稳定性表明，它们将是非酶糖基化的理想底物，非酶糖基化是在高糖含量下长时间发生的过程，最终导致AGEP的形成。这些沉积物还表现出应激反应的证据：HSP72、血红素加氧酶-1和泛素的积累。正如最近的研究所表明的，AGEP修饰的蛋白质会聚集并产生活性氧中间体，这种热休克蛋白的积累可能反映了与AGEP积累相伴的氧化应激，从而促进其细胞功能障碍。因此，有人提出，AGEP与年龄相关的增加，即一个基本的衰老过程，参与了心肌嗜碱性变性和神经胶质细胞淀粉样体的形成。
