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Adolescent idiopathic scoliosis (AIS) is a complex spinal deformity of unknown aetiology and extreme variability, occurring at least in genetically predisposed children. We previously demonstrated a differential dysfunction of melatonin signaling through Gi proteins in osteoblasts from AIS patients, leading to stratification of patients into three functional subgroups. Herein we extended our study to other cell types and various Gi-coupled receptors.

From melatonin to systemic Gi signalling defect: a hopeful odyssey for adolescent idiopathic scoliosis