Estrogen counteracts increased infarct size and cardiac remodelling in post-menopause women with T2D and MI
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.