Catecholaminergic neurons boost fibroblast osteogenic activity in keloid

fibroblasts. Therapeutic interventions targeting catecholamine biosynthesis or adrenergic innervation, and pharmacological inhibition or genetic ablation of ADRB1 effectively prevent keloid-like pathology in a rodent model. Our study provides the demonstration of neuronal-adrenergic signaling driving fibrotic/osteogenic matrix overproduction through TSN-mediated RNA trafficking, revealing therapeutic targets for keloid management.