## 3 Results and Discussion  
### Pax7 as a Key Indicator for Myogenesis  
Pax7, also known as Paired-Box Gene-7, is a transcription factor that belongs to the PAX family and is strongly linked to adult satellite cells, which are precursors of skeletal muscle cells [16; 40]. Satellite cells are derived from embryonic progenitor cells during development, which divide only a limited number of times, whereas adult satellite cell activation induces differentiation, proliferation, and fusion in muscle regeneration, transforming it into myofibers [41; 42]. Quantifying the _Pax7_ gene and/or protein expression as a marker for determining the function of a novel molecular factor at different phases of myogenesis is unavoidable in muscular dystrophy research. _Pax7_-expressing satellite cells are well-established models for determining myoblast activation and myogenic status [43; 44]. _MyoD_ belongs to the basic helix-loop-helix transcription factor family, and is frequently used as a marker for myogenic and activated satellite cell identification in conjunction with Pax7 [44; 45]. _Pax7_ and _MyoD_ interact with each other during myogenesis, making them ideal markers for determining the cells' quiescent, activation and myogenic status. The _Pax7_ and _MyoD_ proportions of satellite cell subpopulations have well-established symmetric expression patterns; Pax7+/MyoD\(-\), Pax7+/MyoD+, and Pax7\(-\)/MyoD+ [44; 46; 47]. The Pax7+/MyoD\(-\) cell population pattern, known as self-renewal satellite cells, highly expresses _Pax7_ to keep the cells quiescent, and is necessary for the maintenance of stem cell homeostasis [43; 48]. Pax7+/MyoD+ cells are activated satellite cells that express myogenic factors and permit the cells to differentiate and proliferate, whereas Pax7\(-\)/MyoD+ cells are differentiating cells that are also controlled by other MRFs [49]. The symmetric expression pattern quantification is also often quantified using _Pax7_ and _Myf5_ instead of _MyoD_. To investigate muscle regenerative capacity, [PERSON] et al. and [PERSON] et al. measured _Pax7_ gene and/or protein expression levels in satellite cells during all phases of myogenesis before and after injury. Differential expression of _Pax7_ as a proliferation marker was observed at different degrees of injury to reveal the state of the satellite cell niche, where [PERSON] et al. discovered that Pax7+ cell number per myofiber in satellite cell-specific conditional knockout mice for _Notch1/Notch2_ (scDKO) is almost entirely ablated compared to control mice after 5 and 19 days of final tamoxifen (TMX) treatment, suggesting impaired muscle regeneration. Pax7+/MyoD\(-\) cell population expansion in scDKO mice was suppressed, which agreed with the reduction of proliferative cells and induced _MyoG_ expression, compared to control mice. [PERSON] et al. investigated the muscle fiber regenerative capacity even after acute injury by observing the exogenous and endogenous expression of _Pax7_, which reflects the self-renewable and myogenic ability of satellite cells at different ages of the mice model. The team quantified the number of Pax7+ cells in tibialis anterior (TA) sections of the mice at different ages, of 6 weeks, 12 weeks, 6 months, and 12 months old, and compared calcium-dependent and phospholipid-dependant protein kinase (PKC0) null mice with the controls. They found that PKC0 null mice showed over 50% more Pax7+ cells than the controls. The presence of Pax7+/MyoD\(-\) and Pax7+/MyoD+ cell populations implied an increase in both quiescent and proliferative cells in PKC0 null mice. Furthermore, [PERSON] et al. discovered that the cell population, Pax7\(-\)/Myf5+, was approximately 25% higher in transmembrane heparan sulphate proteoglycan syndecan-3 (_Sdc3_) null dystrophic mice (Sdc3\(-\)/\(-\)) than in wild-type (WT), indicating that reduced _Pax7_ expression in the absence of _Sdc3_ resulted in a reduction of self-renewable cells.