With increasing life expectations, more and more patients suffer from fractures either induced by intensive sports or other bone-related diseases. The balance between osteoblast-mediated bone formation and osteoclast-mediated bone resorption is the basis for maintaining bone health. Osterix (Osx) has long been known to be an essential transcription factor for the osteoblast differentiation and bone mineralization. Emerging evidence suggests that Osx not only plays an important role in intramembranous bone formation, but also affects endochondral ossification by participating in the terminal cartilage differentiation. Given its essentiality in skeletal development and bone formation, Osx has become a new research hotspot in recent years. In this review, we focus on the progress of Osx’s function and its regulation in osteoblast differentiation and bone mass. And the potential role of Osx in developing new therapeutic strategies for osteolytic diseases was discussed.

The lncRNA BDNF-AS/miR-130b-5p/PRDM5 axis might be a promising therapeutic target for ASCI.

Spinal cord injury (SCI) usually results in neurological damage. DGCR5 is closely related to neurological disorders, and this study aims to explore its role in neuronal apoptosis in acute SCI. The ASCI model was established in rats, and the Basso, Beattie, and Bresnahan (BBB) scoring was used to assess the neurological function. The expression of RNA and protein was quantified by quantitative real-time PCR (qRT-PCR) and western blotting, respectively. The oxygenglucose deprivation (OGD) was performed upon neurons and apoptosis was evaluated by flow cytometry. The interaction and binding between DGCR5 and PRDM5 was detected with RNA pull-down and RIP assay, respectively. DGCR5 was down-regulated in ASCI model rat and in neurons treated with hypoxia. Over-expression of DGCR5 inhibited neuronal apoptosis. Interaction between DGCR5 negatively regulated PRDM5 protein expression by binding and interacting with it. DGCR5 inhibited neuronal apoptosis through PRDM5. Over-expressed DGCR5 ameliorated ASCI in rat. DGCR5 suppresses neuronal apoptosis through directly binding and negatively regulating PRDM5, and thereby ameliorating ASCI.