Hughes, A.Rojas-Canales, D.Drogemuller, C.Voelcker, N.Grey, S.Coates, P.2015-06-252015-06-252014Journal of Endocrinology, 2014; 221(2):R41-R480022-07951479-6805http://hdl.handle.net/2440/92579In the week following pancreatic islet transplantation, up to 50% of transplanted islets are lost due to apoptotic cell death triggered by hypoxic and pro-inflammatory cytokine-mediated cell stress. Thus, therapeutic approaches designed to protect islet cells from apoptosis could significantly improve islet transplant success. IGF2 is an anti-apoptotic endocrine protein that inhibits apoptotic cell death through the mitochondrial (intrinsic pathway) or via antagonising activation of pro-inflammatory cytokine signalling (extrinsic pathway), in doing so IGF2 has emerged as a promising therapeutic molecule to improve islet survival in the immediate post-transplant period. The development of novel biomaterials coated with IGF2 is a promising strategy to achieve this. This review examines the mechanisms mediating islet cell apoptosis in the peri- and post-transplant period and aims to identify the utility of IGF2 to promote islet survival and enhance long-term insulin independence rates within the setting of clinical islet transplantation.en© 2014 Society for Endocrinologyinsulin-like growth factor; apoptosis; islets; cell survival; islet transplantationJournal article003002390710.1530/JOE-13-05570003371109000042-s2.0-84899807065109993Drogemuller, C. [0000-0001-9770-4845]Grey, S. [0000-0003-2160-1625]