Def6 functions as a novel immunoregulator in bone cells via endogenous type-I interferon response to regulate bone remodeling.

miR-335-3p, which targets FOS and inhibits its activation of NFATC1 signaling, is an important regulator for osteoclast function and responsible for the psychological stress-induced osteoporosis.

A comprehensive review focusing on the role of osteoclasts as active regulators of bone homeostasis by influencing osteoblast function explores the currently known mechanisms and coupling factors involved in osteoclast–osteoblast communication and their potential as treatments for bone diseases.

Osteoblast glucose metabolism is impaired in a mouse model for type II diabetes and can be boosted pharmacologically or genetically to alleviate diabetic osteopenia.

It is shown that the absence of the centrosome protein ninein provokes premature ossification during mouse development, due to a defect in the fusion of precursor cells into syncytial osteoclasts.

MMP14 activity-mediated cleavage of the ectodomain of PTH1R modulates PTH signaling in the chondrocyte-derived osteoblast lineage, regulating osteogenesis and thereby bone metabolism, with therapeutic significance for bone-wasting diseases.

Peroxiredoxin 5 contributes to the maintenance of bone homeostasis by regulating osteoblast differentiation.

The loss of miRNA-27a stimulates osteoclast-mediated bone resorption but does not affect osteoblast-mediated bone formation, leading to the development of osteoporosis in mice.

MMnet is a conserved, trans-regulated gene network that controls skeletal homeostasis through osteoclast multinucleation and bone resorptive function.

Rgs12 protein is a novel regulator of the Nrf2 protein by facilitating the proteasomal degradation of the transcription factor during osteoclast differentiation.