De novo myogenesis, or the formation of muscle fibers, begins during the early embryonic stages. The skeletal muscle is formed from somites– blocks of embryonic cell layers. The somites are further divided into dermatomes, myotomes, sclerotomes, and syndetomes. Among these, the myotomes give rise to muscle fibers.
Muscle progenitor cells (MPCs) are formed from the myotomes. MPCs express genes that encode the transcription factors Pax3 and Pax7. Along with Pax 3/7, other transcription factors from the myogenic regulatory factors drive the MPCs into the myogenic lineage. Pax3 activates the expression of the MyoD–a basic helix-loop-helix transcription factor and a strong transactivator. MyoD can transform MPCs and undifferentiated cells, including fibroblasts, into muscle cells such as myoblasts through myogenesis. The dividing myoblasts exit the cell cycle and express genes that transform myoblasts into myofibrils.
Mitochondria play an important role in myogenesis. During myogenesis, cells switch from primarily glycolysis for energy to oxidative phosphorylation to produce the ATP required for myogenesis. Oxidative phosphorylation takes place in the mitochondrial matrix. Additionally, mitochondrial enzymes are highly active during myoblast differentiation and muscle regeneration. Similarly, muscle injury causes a loss of citrate synthase activity, resulting in aberrant muscle regeneration. As the regulatory role of mitochondria in myogenesis is being investigated, mitochondria appear to be promising candidates for the treatment of muscle-related disorders.
