Fig. 3
From: Methylglyoxal, a highly reactive dicarbonyl compound, as a threat for blood brain barrier integrity
Apoptotic pathways after methylglyoxal exposure in brain microvascular endothelial cells. A decrease in cell survival signals and an increase in stress signaling by MGO treatment leads to an imbalance in Bax/Bcl-2, leading to Bax forming pores in the mitochondrial membrane [59, 64]. This leads in consequence to the release of cytochrome C from the mitochondria into the cytoplasm activating the caspase cascade [75] through caspase 9 and consequently also through caspase 3, leading to apoptosis [59, 64, 65]