APEX1, a transcriptional hub for endochondral ossification and fracture repair.

ABSTRACT: After injury, bone tissue initiates a reparative response to restore its structure and function. The failure to initiate or delay this response could result in fracture nonunion. The molecular mechanisms underlying the occurrence of fracture nonunion are not yet established. We propose that hypoxia-triggered signaling pathways, mediated by reactive oxygen species (ROS) homeostasis, control Bmp2 expression and fracture healing initiation. The excessive ROS leads to oxidative stress and, ultimately, fracture nonunion. In this study, we silenced Apex1, the final ROS signaling transducer that mediates the activation of key transcription factors by their cysteines oxidoreduction, evaluating its role during endochondral ossification and fracture repair. Silencing Apex1 in limb bud mesenchyme res

SUBMITTER: Valdes-Fernandez J 

PROVIDER: S-EPMC12811256 | biostudies-literature | 2026 Jan

REPOSITORIES: biostudies-literature