Type 2 diabetes mellitus (T2D) leads to an increased infarct size in postmenopausal women. The G protein-coupled estrogen receptor (GPER) may be decisive here. This oestrogen receptor mediating rapid non-genomic effects. Its expression is reduced both during menopause and in T2D. This is of great relevance as GPER is protective in myocardial infarction. We hypothesize that estrogen as a GPER activator in the infarct is therefore a potential therapeutic target. This will be investigated in murine analyses in the menopausal model with T2D and infarction. Additionally, in an observational patient study, estrogen levels and GPER expression will be associated with infarct size in postmenopausal women with T2D.

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