Catalpol facilitated bone regeneration and vessel formation in a calvarial defect rat model with OVX-induced osteoporosis and promoted the osteogenic ability of BMSCs and BMSC-dependent angiogenesis through by activating the JAK2/STAT3 axis; these benefits could be partially abolished by knocking down STAT3 [69]. This evidence concerns the gene STAT3 and osteoporosis.