IDH2-deficient mice develop spinal deformities with aging.

摘要

Spinal deformities such as scoliosis and kyphosis are incurable,and can lead to decreased physical function, pain, and reducedquality of life. Despite much effort, no clear therapies for thetreatment of these conditions have been found. Therefore, thedevelopment of an animal model for spinal deformity would beextremely valuable to our understanding of vertebral diseases. Inthis study, we demonstrate that mice deficient in themitochondrial enzyme isocitrate dehydrogenase 2 (IDH2) developspinal deformities with aging. We use morphological analysis aswell as radiographic and micro-CT imaging of IDH2-deficient miceto characterize these deformities. Histological analysis showedincreased abnormalities in IDH2-deficient mice compared to wildtype mice. Taken together, the results suggest that IDH2 playsa critical role in maintaining the spinal structure by affecting thehomeostatic balance between osteoclasts and osteoblasts. Thisindicates that IDH2 might be a potent target for the developmentof therapies for spinal deformities. Our findings also providea novel animal model for vertebral disease research.