IGF2: An endocrine hormone to improve islet transplant survival

Amy Hughes, Darling Rojas-Canales, Chris Drogemuller, Nicolas H. Voelcker, Shane T. Grey, P. T.H. Coates

Research output: Contribution to journalReview articlepeer-review

18 Citations (Scopus)
32 Downloads (Pure)


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.

Original languageEnglish
Pages (from-to)R41-R48
Number of pages8
JournalJournal of Endocrinology
Issue number2
Publication statusPublished - May 2014
Externally publishedYes


  • Apoptosis
  • Cell survival
  • Insulin-like growth factor
  • Islet transplantation
  • Islets


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