Linn T, Schmitz J, Hauck-Schmalenberger I, Lai Y, Bretzel R G, Brandhorst H, Brandhorst D
Medical Clinic and Policlinic 3, University Hospital Giessen and Marburg, Justus Liebig University, Rodthohl 6, 35385 Giessen, Germany.
Clin Exp Immunol. 2006 May;144(2):179-87. doi: 10.1111/j.1365-2249.2006.03066.x.
Beta-cell replacement is the only way to restore euglycaemia in patients with type-1 diabetes. Pancreatic tissue, processed for subsequent clinical islet transplantation, is exposed to ischaemia causing injury and death in a large number of islets before and after transplantation. In this review we summarize what is known on the sources of environmental stress for pancreatic islets, such as insufficient oxygen supply during pancreas procurement and in culture prior to intraportal transplantation, nutritional and oxygen deprivation during the isolation process, and the consequences of hyperglycaemia. An increasingly recognized role in the modulation of beta-cell function and these environmental stress factors plays the vascular network of the pancreatic islets. Islet revascularization by angiogenesis is relevant for the survival of the graft subsequent to transplantation. Potential strategies offered by therapeutic induction of revascularization to ameliorate the detrimental impact of these factors on the quality of islet transplants are discussed.
β细胞替代是恢复1型糖尿病患者血糖正常的唯一方法。为后续临床胰岛移植而处理的胰腺组织,在移植前后会暴露于缺血环境中,导致大量胰岛受损和死亡。在本综述中,我们总结了已知的胰岛环境应激源,如胰腺获取过程中及门静脉内移植前培养期间的氧气供应不足、分离过程中的营养和氧剥夺,以及高血糖的后果。胰岛的血管网络在调节β细胞功能和这些环境应激因素方面发挥着越来越重要的作用。移植后通过血管生成实现胰岛再血管化与移植物的存活相关。本文讨论了通过治疗性诱导再血管化来减轻这些因素对胰岛移植质量的不利影响的潜在策略。