Searching new molecular targets in Fibrodysplasia Ossificans Progressiva (FOP): is the autophagy signalling a good candidate?

Fibrodysplasia ossificans progressiva (FOP) is a hereditary form of heterotopic ossification (HO). FOP is due to a heterozygous mutation in the ACVR1 gene that lead to constitutive activation of mutant ACVR1, involved in HO. Hypoxia environment is crucial in the induction of HO in FOP and sustains mutant ACVR1 constitutive signalling. Despite this, the molecular mechanism involved in adaptation to hypoxia environment and that contribute to mutant ACVR1 signalling in FOP are still largely unknown. In this project, we hypothesize that autophagy signalling, could be involved in hypoxia induction of HO and in sustaining mutant ACRV1 signalling. This study could contribute to find new molecular “actors” involved in FOP progression, and so could lead to the design new molecular target therapy for FOP.