## 3 Results and Discussion
### Pax7 in the Context of Embryonic, Fetal, and Adult Myogenesis  
Muscle development occurs as a sequential event, starting with embryonic, to fetal, and ending with adult myogenesis. The majority of embryonic myoblasts and satellite cells contain Paired-Box Gene-3 (Pax3), a member of the PAX family of transcription factors, which is a pivotal gene involved in organ development [13; 54]. Satellite cells which are capable of self-renewal and myogenic differentiation facilitate postnatal muscle formation and regeneration. The remnants of embryonic-origin _Pax7_-expressing cells from development give rise to post-embryonic myogenesis, and are required for fetal myogenesis as well as adult skeletal muscle regeneration, which is critical for skeletal muscle repair. Using a dyW mice model, which is derived from homologous recombinant in mouse embryonic stem (ES) cells with laminin alpha 2 (_Lama2_)-knockout [55], [PERSON] et al. explored the _merosin_-deficient congenital muscular dystrophy type 1A (MDC1A) to trace the advent of the disease during muscle development in utero. They observed the homozygous dyW mice embryo to have significantly smaller muscle than the wild type at the fetal age of E15.5 to E18.5, although expressing the same number of myofibers. They discovered that the increase in the Janus kinase/signal transducers and activators of the transcription (JAK-STAT) signaling pathway, together with the decreased expression of _myostatin_ and _Pax7_, caused the satellite cells to lose their normal level of self-renewal capacity. [PERSON] et al. also discovered an increase in _MyoD_ expression at E18.5, as the cells exited the cell cycle faster, and reduced the differentiation and fusion rate. dyW mice had an aging phenotype that could not recover during the development event, due to low _Pax7_ levels, reflecting a low level of self-renewal capacity. Fetal myogenesis is closely associated with the formation of myofibers (hyperplasia) and myofiber fusion (hypertrophy). Improper execution of this sequential event may result in fewer differentiated and competent cells in utero. [PERSON] et al. investigated the muscle development stage in mice model fetuses and muscular biopsies from 12-week-old DMD and healthy human fetuses, using histological evaluation. They revealed a decrease in fiber density, where dystrophic fetal muscles expressed significantly higher levels of fast-type genes such as sarcoplasmic reticulumATGase-1 (_ATP2A1_), troponin T type 3 (_TNNT3_) and troponin fast C Type 2 (_TNNC2_). Dystrophic muscle is known to have dystrophin protein loss, which causes membrane tears and sarcolemmal destabilization, resulting in abnormal Ca2+ reflux [56; 57]. [PERSON] et al. examined myogenic marker expression in 12-week-old healthy and DMD human fetal muscles, and discovered a significantly higher number of Pax7+ cells per myofiber in DMD samples compared with healthy. _PKCa_ is a serine/threonine kinase belonging to the PKC family, and it is involved in numerous cellular processes. In human fetal dystrophic muscle, _PKCa_ is upregulated, and its activity is regulated by Ca2+ levels, contributing significantly to muscle development and plasticity. They hypothesized that inositol 1,4,5-trisphosphate (IP3)-IP3R binding-mediated Ca2+ signaling determines calcium cell accumulation in DMD muscle. [PERSON] et al. discovered that enhanced _PKCa_ activation causes altered myogenesis in DMD muscles, by overexpressing _Pax7_ while suppressing _MyoD_, along with a delay in fiber maturation and a modification in fiber type composition. Therefore, by attuning the IP3/IP3R pathway, satellite cells could exit the stemness state and express myogenic markers accordingly, during myogenesis, for the next regeneration cycle, and limit DMD muscle damage by Ca\({}^{2+}\) deposition. [PERSON] et al. in their research in 2016 demonstrated the extracellular matrix (ECM) function in muscle stem cell regulation at different stages of muscle development.