Elaidic acid leads to mitochondrial dysfunction via mitochondria-associated membranes triggers disruption of mitochondrial calcium fluxes

Elaidic acid (EA) stimulation can lead to endoplasmic reticulum stress (ERS), accompanied by a large release of Ca2+, and ultimately the activation NLRP3 inflammasome in Kupffer cells (KCs). Mitochondrial instability or dysfunction may be key stimulating factors activate inflammasome, sustained Ca2+ transfer result mitochondrial dysfunction. We focused on KCs explore damage mitochondria EA. After EA stimulation, produced an oxidative (OS) response with significant increase ROS release. Immunoprecipitation experiments addition inhibitors revealed that level intracellular led accumulation matrix via mitochondria-associated membranes (MAMs). This was mROS, loss MMP ATP, permeability transition pore opening, leading instability. These findings confirmed mechanism induced imbalance MAM, Meanwhile, OS decrease ATP rat liver, lesions were found liver mitochondria. Swelling inner cristae vacuolization occurred, marked lipid droplets.