**1. Introduction**

In physiological conditions, the adult skeletal muscle has a relatively low cell turnover [1]. However, physical activity, trauma, or muscle pathologies, undermining tissue integrity, trigger a tightly controlled regeneration process. Although satellite cells (SCs) are the main actors of myofiber regeneration after damage [2–6], successful muscle healing requires the participation of additional cell types that directly or indirectly contribute to this process. In this context, immune cells and fibro/adipogenic progenitors (FAPs) play a prominent role in supporting the clearance of the damaged tissue, while assisting SCs in their regenerative role [7–11]. However, the orchestrated crosstalk of the regeneration machinery gradually fails in patients affected by muscle-related disorders, such as dystrophies [12]. Here, the accumulation of intrinsic cell defects and the changes in the stem cell niche lead to infiltrations of fat and fibrotic deposition, compromising muscle functions [9,13–16].

Over the past decades, the complex cell crosstalk occurring during muscle regeneration has been studied in detail [17–19]. However, to date, most studies have mainly relied on the analysis of bulk cell populations identified by the expression of a few specific markers and sorted for ex vivo analysis. As a consequence, due to the lack of technologies suitable to address this issue, little is known about muscle cell population heterogeneity. Only recently, the development of technologies to determine the transcriptome of single-cells or their exposed antigen repertoires has permitted to reveal the extent of this heterogeneity and its possible implication in muscle physiology and pathology [20–24]. Moreover, the dynamic changes and the relative abundance of muscle cell populations, upon acute or chronic damage, still remain largely uncharacterized. To fill this gap, we explored, via single-cell mass cytometry, the changes in the multidimensional antigen repertoires of the main players, colonizing the muscle stem cell niche after injury. Here, we described, at single-cell resolution, the time-dependent changes of muscle population dynamics upon myotoxin-induced damage in wild type (wt) and in a mouse model of Duchenne muscular dystrophy (the mdx model).
