Therefore, MSCs may improve mitochondrial dysfunction through PINK1/Parkin-mediated mitophagy, thereby protecting endothelial cells from damage caused by hyperglycemia [47, 48] The upregulation of Parkin expression and downregulation of p53 expression in BMSCs can significantly enhance the mitophagy ability of BMSCs and reduce the accumulation of damaged mitochondria in cells, effectively resisting stress-induced apoptosis and senescence of BMSCs and improving the effect of BMSCs transplantation on hormone-induced early ONFH (osteonecrosis of the femoral head) [48]. This evidence concerns the gene PRKN and Hyperglycemia.