SPP1 and neuromuscular disease caused by qualitative or quantitative defects of dystrophin: Summarizing the findings on osteopontin in animal models of muscle disease, it appears that muscle damage strongly induces osteopontin, probably through nuclear factor κB (NF-κB) responsive elements in the promoter; that its absence delays tissue repair in models of acute damage, but conversely reduces fibrosis due to the chronic damage that is caused by dystrophin deficiency; and that, ultimately, it is involved in different phases of muscle remodeling with various, sometimes contrasting, pro-inflammatory and pro-regenerative effects [37].