In our aging society, degenerative complications of chronic diseases are on the rise and account for a significant percentage of deaths. Among these, fibrosis is the most common, and yet no therapy capable of mitigating its effects is available. Investigating and understanding the signaling pathways that influence fibrogenic progenitor (FAP) fate will not only elucidate a key component of the regenerative process but may reveal pathways that could be targeted therapeutically to prevent inflammation, fibrosis, and enhance regeneration or maintain muscle homeostasis.
Here, we will focus on the ability of these progenitors to attract to damaged tissues specific inflammatory cells (eosinophils) that have been linked to fibrosis, with the goal of learning how to prevent their excessive accumulation and thus prevent this prevalent complication of muscular dystrophies and other chronic diseases.