Brownlee M
Department of Medicine, Albert Einstein College of Medicine, Bronx, New York 10461.
Annu Rev Med. 1991;42:159-66. doi: 10.1146/annurev.me.42.020191.001111.
Hyperglycemia causes excessive amounts of irreversible advanced glycosylation end products (AGEPs) to accumulate on long-lived extracellular matrix proteins and probably also on DNA in tissues that develop diabetic complications. AGEPs induce permanent abnormalities in extracellular protein cross-linking, cell-matrix interactions, and DNA structure in vitro. Pharmacologically inhibiting AGEP formation in long-term diabetic animals prevents both retinal capillary pathology and thickening of the glomerular basement membrane.
高血糖会导致大量不可逆的晚期糖基化终末产物（AGEPs）在长寿的细胞外基质蛋白上积累，并且可能也会在发生糖尿病并发症的组织中的DNA上积累。AGEPs在体外会诱导细胞外蛋白质交联、细胞-基质相互作用和DNA结构的永久性异常。在长期糖尿病动物中通过药物抑制AGEP的形成可预防视网膜毛细血管病变和肾小球基底膜增厚。
