IGF2: an endocrine hormone to improve islet transplant survival
In 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.
|Authors||Hughes, A.; Rojas-Canales, D.; Drogemuller, C.; Voelcker, N. H.; Grey, S. T.; Coates, P. T.|
|Publisher Name||JOURNAL OF ENDOCRINOLOGY|
|OpenAccess link to author's accepted manuscript version||https://publications.gimr.garvan.org.au/open-access/12183|