Malat1 is a key skeletal regulator, unveiling how lncRNAs integrate cellular crosstalk and molecular networks to regulate bone remodeling and regeneration, establishing a novel paradigm in tissue homeostasis and repair.
Cartilage and bone tumors arise from chondrocyte or osteoblast progenitors but not differentiated cells or multipotent mesenchymal stem cells (MSCs) via the IHH-Wnt/β-Catenin pathway.
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.
Mir155 showed a catabolic effect on osteogenesis and bone mass phenotype via interaction with the S1pr1 gene, suggesting inhibition of Mir155 as a potential approach to bone regeneration and bone defect healing.
Transferrin receptor 1-mediated iron uptake plays a pivotal role in osteoclast energy metabolism and cytoskeleton and regulates bone remodeling in female mice.
Targeted SOCS3 null mice reveal that maturation of cortical bone comprises both pore closure and accumulation of high density bone, requiring local suppression of gp130-STAT3 in osteocytes and subsequent osteoclastogenesis.
