cGAS-STING Pathway Mediation in Osteoclast Function and Bone Fracture Healing
Inflammation, as a crucial initial phase of bone healing, typically commences in the early stages of fracture repair. The cGAS-STING pathway serves as a key mediator of inflammation. The aim of this study is to explore the biological role and molecular mechanisms of the cGAS-STING pathway in the fracture healing process, with a particular focus on its function during the early inflammatory phase. Overall design: A murine femoral fracture model was utilized to investigate the activation of the cGAS-STING pathway during the early and late stages of bone healing. The methodologies encompassed transcriptome sequencing and immunohistochemistry. Pathway modulation was accomplished through the application of the STING inhibitor H-151 and the activator SR-717, with the effects being assessed via in vivo experiments (transcriptome sequencing, microCT, safranin O-fast green staining, and TRAP staining) and in vitro assays (TRAP staining, F-actin ring formation, bone resorption tests, qPCR, and Western blot analysis).