Perivascular extracellular vesicles induce bone repair, and do so via tetraspanin binding to recipient skeletal progenitor cells.

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.

Short-term interventions, including intermittent fasting, boosting cellular energy, and promoting beneficial gut bacteria, rejuvenate osteoprogenitors in aged animals and, when combined with localized Wnt, restore youthful bone healing.

A single-nucleus atlas of bone repair uncovers the trajectories of periosteal skeletal stem/progenitor cells in response to fracture and identifies injury-induced fibrogenic cells as intermediate osteochondroprogenitors and key paracrine regulators.

Activation of Activin A-expressing progenitor cells emerges as a pivotal mechanism in bone fracture healing, shedding light on a potential therapeutic avenue to augment bone repair processes.

High-resolution multiphoton microscopy reveals coupling of blood vessel subtype with expanding osteoblasts at the bone regeneration interface, further highlighting the heterogeneity of oxygen microenvironment and its impact on cellular energy metabolism of bone and vessel forming cells.

Bone cells exposed to physiological forces release ATP through repairable membrane injury, generating an intercellular signal that conveys the destructive potential of forces and the adaptive capacity of endangered cells.

Large-scale skeletal regeneration requires Hh signaling in Sox9+ lineage cells to coordinate callus formation and bone repair.

Ablation of the Cdkn1c cell cycle inhibitor leads to defective muscle stem cell dynamics and myogenic potential, while progressive cytoplasmic to nuclear cellular localization of the Cdkn1c protein regulates growth arrest.

A periosteal Bmp2 signaling center couples bone length to bone width during development and must be reactivated by clinical bone anabolic therapies to reduce fracture risk and accelerate fracture repair.