## 4 Conclusions  
Overall, _Pax7_ plays a critical role in muscle development, and contributes to skeletal muscle repair through its regenerative function. In terms of signaling pathways, research on _Pax7_ expression levels indicates its interaction with the Notch and Wnt pathways during myogenesis. This interaction is vital for regulating the cell fate and behavior of muscle stem cells, underscoring the complex regulatory network involved in muscle formation and repair. However, when it comes to muscular dystrophy, there is a lack of information regarding _Pax7_'s specific role at various stages of the disease progression. Investigating _Pax7_'s function at these specific time-points could prove to be a fascinating area of study, potentially revealing whether modulating _Pax7_ expression levels at these stages would impact the severity and progression of the disease. By gaining a deeper understanding of how _Pax7_ interacts with other signaling pathways, we hope that future research can uncover the underlying mechanisms involved in myogenic programming. This insight could open new avenues for manipulating _Pax7_ expression, leading to potential therapeutic strategies for treating muscle-related conditions. Realistically, relying solely on _Pax7_ as a therapeutic target in muscular dystrophy treatment would be challenging, due to the diverse forms of muscular dystrophy and their respective genetic mutations. Muscular dystrophies, despite their different underlying causes, share a common characteristic of progressive muscle wasting, in which _Pax7_ could play a crucial role. Utilizing _Pax7_'s regulatory function could be advantageous, particularly in combination with existing approaches in muscular dystrophy therapy. In the case of dystrophinopathies, _Pax7_ cannot address the lack or complete absence of _ dystrophin_. However, it could be used as a complementary approach to support _ dystrophin_ rescue efforts. Similarly, in Facioscapulohumeral muscular dystrophy, inducing _Pax7_ overexpression in regions where it is repressed might hold the potential to ameliorate disease pathology [85]. Additionally, while _Pax7_ shows promise as a valuable player in mitigating muscle wasting, it is more practical to view it as part of a comprehensive approach in combination with other therapeutic strategies, for addressing the complexities of muscular dystrophy effectively. By understanding and harnessing _Pax7_'s regulatory potential, we can enhance current therapeutic efforts and pave the way for more effective treatments for various forms of muscular dystrophy. Furthermore, it would be essential to investigate whether muscular dystrophy models undergoing treatment via pharmacological strategies could benefit from the regenerative potential of _Pax7_ overexpression when induced. Understanding the mechanistic and synergistic effects of _Pax7_ in combination with existing therapies could potentially refine and complement current therapeutic strategies. Ultimately, this could alter the direction and dynamics of the treatment method for muscular dystrophy, and a hopeful solution brought from the bench to bedside. \begin{table}
\begin{tabular}{c c c c c} \hline \hline
**No. Author(s)** & \ \begin{tabular}{c} **Year of** \\ **Publication** \\ \end{tabular}  & **Animal Model** & \begin{tabular}{c} **Signaling** \\ **Pathways** \\ \end{tabular}  & & \multicolumn{1}{c}{**Key Findings**} \\ \hline \hline
7 & \begin{tabular}{c} Mu et al. \\ [39] \\ \end{tabular}  & 2015 & \begin{tabular}{c} Wild-type (C57 BL/[10] background), \\ mdx (dys\({}^{-/-}\)) and dKO \\ (dys\({}^{-/-}\),atm\({}^{-/-}\)) mice \\ \end{tabular}  & \ \begin{tabular}{c} Notch and \\ TGF-\(\beta\) \\ (dys\({}^{-/-}\),atm\({}^{-/-}\)) mice \\ \end{tabular}  &
\begin{tabular}{c} 1. \\ 2. \\ 3. \\ 3.