## 3 Results and Discussion
### Pax7 in the Context of Embryonic, Fetal, and Adult Myogenesis
Myogenesis regulation in prenatal muscle stem cells focuses primarily on cellular contribution to myofibers, laying the foundation for subsequent muscle growth. Conversely, in postnatal or adult muscle stem cell myogenesis, the regulation is more focused on the balance between muscle growth and repair, as well as the maintenance of the stem cell pool population for the next regeneration. Fetal muscle stem cells adapt to the microenvironment by autonomously secreting ECM. This leads to stem cell expansion support and enhances stem cell function intrinsically by actively dividing and maintaining the _Pax7_ expression level in growing conditions. They revealed that in differentiation conditions, _Pax7_ expression increased while _Myf5_ and _MyoG_ expression decreased, showing that fetal muscle stem cells resist myogenic lineage progression. This implies that fusion efficiency increases during development. Fetal muscle stem cells expressed higher level of Notch targets and a reduced level of canonical Wnt targets, compared to activated adult muscle stem cells, suggesting innate and robust expansion. Adult muscle stem cells profited from co-transplantation of fetal and adult muscle stem cells by boosting _Pax7_ expression. ECM molecule remodeling was influenced by fetal stem cells in a paracrine manner, improving adult stem cells' regenerative potential for long-term self-renewal, implying that fetal muscle stem cells are responsible for local microenvironmental remodeling and promoting neighboring adult muscle stem cells' regenerative potential. They concluded that fetal muscle stem cells have enhanced regenerative potential during tissue repair and the ability to repopulate the stem cell pool during development. Fetal muscle stem cells possess remarkable regenerative potential through more efficient expansion and selective expression of ECM proteins to remodel their local microenvironment. In a context of adult myogenesis, [PERSON] et al. investigated how satellite cell number and activity decline with age in the mdx mice model. The mdx model is a universal mice model used as DMD murine strain with a point mutation in the _dystrophin_ gene, and exhibits DMD phenotypes [58; 59; 60]. They found that mdx mice expressed higher _Pax7_ than in the wild-type, at different age groups. Their findings were suggested severe age-dependent deficiencies in satellite cell activation and/or proliferation, causing the mice to have reduced satellite cell self-renewal capacity, due to ongoing muscle injuries. Mdx mice had a decrease in Pax7+/MyoD\(-\) cells but an increase in MyoG+/MyoD+ cells, indicating terminal differentiation. They demonstrated that aberrant Notch signaling, which was supposed to be activated and improve the self-renewal capacity, was actually responsible for defective satellite cell renewal in dystrophic muscles. _Dystrophin_ and the Notch signaling cascade may be perturbed in mdx mice satellite cells in dystrophic muscles, as they play an important role in embryonic muscle formation and postnatal myogenesis. The Notch signaling pathway is inhibited in dystrophic muscle satellite cells, leading to a defective self-renewal capacity and potential side effects. The research demonstrated the significance of quantifying _Pax7_ in the sequential event of myogenesis from embryonic and fetal, to adult myogenesis, to understand the relevance of certain signaling pathways and the role of a novel molecular factor in the rescue of dystrophic muscle.