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Interventional Strategies to Prevent ß-Cell Apoptosis in Islet Transplantation

¹ Department of Surgery, University of Alberta, Edmonton, Alberta, Canada
² Clinical Islet Transplant Program, University of Alberta, Edmonton, Alberta, Canada

Address correspondence and reprint requests to Juliet Emamaullee, PhD, 1074 Dentistry-Pharmacy Centre, Surgical Medical Research Institute, University of Alberta, Edmonton, AB T6G 2N8. E-mail: juliete{at}ualberta.ca

Abbreviations: cFLIP, cellular FLICE-inhibitory protein; DISC, death-inducing signaling complex; FADD, Fas-associated death domain; IBMIR, instant blood-mediated inflammatory reaction; IL-1ß, interleukin-1ß; NF-B, nuclear factor-B; ROS, reactive oxygen species; TNF, tumor necrosis factor; XIAP, X-linked inhibitor of apoptosis protein

A substantial proportion of the transplanted islet mass fails to engraft due to death by apoptosis, and a number of strategies have been explored to inhibit ß-cell loss. Inhibition of extrinsic signals of apoptosis (i.e., cFLIP or A20) have been explored in experimental islet transplantation but have only shown limited impact. Similarly, strategies targeted at intrinsic signal inhibition (i.e., BCL-2) have not yet provided substantial improvement in islet engraftment. Recently, investigation of downstream apoptosis inhibitors that block the final common pathway (i.e., X-linked inhibitor of apoptosis protein [XIAP]) have demonstrated promise in both human and rodent models of engraftment. In addition, XIAP has enhanced long-term murine islet allograft survival. The complexities of both intrinsic and extrinsic apoptotic pathway inhibition are discussed in depth.

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