LAUSR

New drug target identified for βcell dysfunction βCell dysfunction characterises type 2 diabetes mellitus (T2DM) and ageing. New research in Nature Metabolism identified microsomal prostaglandin E synthase-2 (mPGES2) as a factor that could be targeted to potentially improve βcell function in T2DM. Global knockdown of Mpges2 in mice that were challenged with a highfat diet or bred with a genetic model of T2DM (db/db mice) improved βcell identity, decreased βcell senescence, increased glucose stimulated insulin secretion and improved glucose homeostasis compared with mice with wild type Mpges2. Further investigation of the mechanisms showed that mPGES2 activates a prostaglandin E2–EP3–NR4A1 signalling axis that induces βcell senescence. Importantly, the researchers discovered an mPGES inhibitor (SZ0232) that could improve glucose tolerance in db/db mice. Further research is necessary to investigate the clinical potential of SZ0232 as a treatment for T2DM.