FAP and Duchenne muscular dystrophy: While chronic inflammation is a known driver of fibrotic remodeling in DMD [9], the direct link between FAP activation and progenitor depletion in human organoids remains speculative and requires functional validation [72] Our previous comprehensive cell–cell communication analysis of healthy skeletal muscle organoids revealed that myogenic progenitors receive prominent ECM-related signals from fibro-adipogenic progenitors, while FAPs respond to signals from activated myogenic progenitors [38].