Abstract
Growing evidence suggests that maternal obesity predisposes offspring to cardiometabolic disorders. In this context, previous studies point to a possible role of mitochondrial and endoplasmic reticulum (ER) dysfunction in the oocyte. In parallel, human and mouse studies report that metabolic diseases mitigate mitofusin2 (MFN2) expression, impacting mitochondria-ER contact sites (MERCs) in…