Thrombosis and Inflammation in Intraportal Islet Transplantation: A Review of Pathophysiology and Emerging Therapeutics
Thrombosis and Inflammation in Intraportal Islet Transplantation: A Review of Pathophysiology and Emerging Therapeutics
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DOI：
10.1177/193229680800200502
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发表时间：
2008-09
影响因子：
5
通讯作者：
John T. Wilson;E. Chaikof
中科院分区：
文献类型：
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作者：
John T. Wilson;E. Chaikof
随着埃德蒙顿协议的开始，门静脉内胰岛移植（IPIT）重新成为一种有前途的1型糖尿病细胞治疗方法。然而，目前的临床胰岛移植仍然有限，部分原因是需要从2-4个供体器官移植胰岛，通常通过多次单独输注，才能在单个患者中逆转糖尿病。临床胰岛移植和实验动物模型的结果表明，大多数移植的胰岛在移植后立即被破坏，这一过程在很大程度上是由胰岛衍生的促凝剂和促炎介质引发的有害炎症反应促进的。本文综述了IPIT中血栓形成和炎症的病理生理机制，并讨论了通过减弱炎症反应来改善胰岛植入的新方法。
With the inception of the Edmonton Protocol, intraportal islet transplantation (IPIT) has re-emerged as a promising cell-based therapy for type 1 diabetes. However, current clinical islet transplantation remains limited, in part, by the need to transplant islets from 2–4 donor organs, often through several separate infusions, to reverse diabetes in a single patient. Results from clinical islet transplantation and experimental animal models now indicate that the majority of transplanted islets are destroyed in the immediate post-transplant period, a process largely facilitated by deleterious inflammatory responses triggered by islet-derived procoagulant and proinflammatory mediators. Herein, mechanisms that underlie the pathophysiology of thrombosis and inflammation in IPIT are reviewed, and emerging approaches to improve islet engraftment through attenuation of inflammatory responses are discussed.