## 3 Results and Discussion
### The Signaling Pathways Underlying Satellite Cell Regulation
#### 3.3.2 Wnt  
Wnt signaling regulates various biological processes, including cell migration, polarity, and motility, and is critical for embryonic formation and development as well as tissue homeostasis in adults [66; 67]. Wnt signaling is a pleiotropic signal that regulates various biological processes, including cell migration, polarity, and motility. It is critical for embryonic formation and development, as well as adult tissue homeostasis [66; 67; 68; 69]. Concisely, Wnt signaling diverges into canonical and non-canonical pathways. The canonical \(\beta\)-catenin pathway, also known as the Wnt/\(\beta\)-catenin pathway, regulates cell proliferation by activating target genes in the nucleus via TCF/LEF protein. The non-canonical pathway branches further into two main pathways: 1. the planar cell polarity pathway that coordinates cellular assembly by controlling cell migration, polarity, and asymmetric division, and 2. a calcium-dependent pathway, which is also known as Wnt/Ca\({}^{2+}\) pathway [66; 67; 69; 70]. \begin{table}
\begin{tabular}{c c c c c} \hline \hline \multicolumn{1}{c}{**No.**} & \multicolumn{1}{c}{**Author(s)**} & \multicolumn{1}{c}{**Year of Publication**} & \multicolumn{1}{c}{**Animal Model**} & \multicolumn{1}{c}{**Key Findings**} \\ \hline \hline
6 & [PERSON] et al. [26] & 2016 & \(MylT^{\text{Cre}}\), Ckmm-Cre (MCK-Cre), \(Rosa26\)(Gt)Sor\({}^{\text{NiICD}}\), \(Rosa26\)(Gt)Sor\({}^{\text{S+Tomato}}\), \(Rosa26\)(Gt)Sor\({}^{\text{MTEG}}\), mdx, and CpGFP mice. & 1. & The study explored the stage-specific effects of Notch activation during skeletal myogenesis. 2. & _Notch1_ activation can revert de-differentiated myocytes back into Pax7+ quiescent stem cells. 3. & In MLC-N1 ICD mice: \(\bullet\) High expression of Pax7+ cells. 4. & In MKC-N1 ICD mice: \(\bullet\) No de-differentiation. \(\bullet\) _Notch1_ activation and enhanced muscle function and regeneration in aged mice. 5. & _Notch1_ activation is stage-dependent in post-differentiation muscle cells. 6. & It improves myotube’s role as a stem cell niche, supporting muscle regeneration and function. \\ \hline
7 & [PERSON] et al. [27] & 2014 & \(MylT^{\text{PLLAZ}}\), \(ROSA26^{\text{NiICD}}\), mdx, Pax7 CreER, and Cp-GFP mice & 1. & The study revealed that age-dependent depletion of satellite cells in muscular dystrophy is attributed to Notch signaling deficiency. 2. & Mdx mice expressed higher \(Pax7\) levels compared to wild type, at all ages. 3. & Young mdx mice showed down-regulated Notch markers. 4. & Impaired Notch signaling affects the ability of cells to self-renew and revert to a quiescent state in aged mice. 5. & Notch inhibits _MyQD_ and _myogenin_, leading to an absence of myogenic differentiation. 6. & Notch activation improves Pax7+ expression, suggesting that fine-tuning of Notch signaling is essential in myogenesis. \\ \hline
8 & [PERSON] et al. [28] & 2013 & \(Numblike\) (\(Nbl^{-/-}\)), conditional \(Numb\) mutant (\(Numb^{\text{fl}/\delta}\)), \(Pax7\)-Cre (\(Pax7\)Ckm), \(R26\)RYF, \(Numb^{\text{PLLAZ}/\text{PLLAZ}}\), \(J\), and the TMX-inducible Cre recombinase line \(CAGE\)\(ER\)-Cre mice & 1. & The study showed that Numb-deficient satellite cells exhibit defects in regeneration and proliferation. 2. & Absence of Numb in the Pax7-lineage: \(\bullet\) Reduced satellite cells on single-fiber culture. \(\bullet\) Causes a defective repair response in adult muscle. 3. & Numb deficiency does not substantially alter expression levels of _MyQD_, _Pax7_ and _Notch_ ligands in satellite cells. 4. & Notch signaling is not the primary mechanism regulating satellite cell proliferation. 5. & Silemcing _Myostatin_ rescues proliferation in Numb-deficient mice. \\ \hline \hline \end{tabular}
\end{table} 
Table 2: _Cont._[PERSON] et al. in their 2014 report, investigated the Wnt signaling pathway activation in mice models using voluntary wheel running as a mild physiological stimulus.