“…Recently, some researchers demonstrated that the increased mitochondria-associated endoplasmic reticulum membrane (MAM) formation is sufficient to trigger premature cellular senescence, involving a mitochondrial ROS/p53 pathway and a partial NFκB-dependent SASP induction . The outer mitochondrial membrane (OMM) in the dynamic network of mitochondria through a special structure known as the MAM, communicates with the endoplasmic reticulum membrane. − Besides, MAM dynamic formation regulates mitochondrial dynamics, autophagy, inflammation, and apoptosis in addition to being implicated in lipid metabolism, calcium signaling, and redox signaling . Therefore, this study was designed to explore the relationship between MAM-related genes and cellular senescence-related genes in OA.…”