JCI Insight · 7 authors, 7 centres
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This preclinical study used mouse models and cell experiments to show that glutathione protects the bone-forming transcription factor RUNX2 from oxidative degradation. When glutathione is limited, RUNX2 is degraded, leading to impaired osteoblast differentiation and reduced bone formation.
The central finding is that de novo GSH biosynthesis is essential for neutralizing ROS and establishing a proosteogenic REDOX environment. Conversely, reducing ROS with catalase stabilized RUNX2 and rescued osteoblast differentiation even when GSH was limited. In a mouse model of cleidocranial dysplasia (Runx2 haploinsufficiency), in utero antioxidant therapy stabilized RUNX2 and improved bone development. The findings imply that metabolic strategies targeting GSH synthesis or ROS scavenging could be potential therapeutic avenues for conditions of low bone mass.
