Regulating islet stress responses through CD47 activation.

ABSTRACT:

Aims/hypothesis

Diabetes is a global health burden characterised by incremental beta cell loss. Islet transplantation is a recognised treatment for individuals with type 1 diabetes and hypoglycaemia unawareness but broader application is constrained by limited islet survival and function post-transplantation. The underlying molecular mechanisms that induce beta cell dysfunction and demise remain unclear, and therapeutic agents that protect against cellular loss and maintain insulin secretion are in demand as potential treatment options. CD47 is a cell surface protein implicated in cellular stress responses but its role in beta cell function remains relatively unexplored. We hypothesised that modulating CD47 expression would demonstrate a cytoprotective effect in beta cells.

Meth

SUBMITTER: Kale A 

PROVIDER: S-EPMC12069481 | biostudies-literature | 2025 Jun

REPOSITORIES: biostudies-literature