Satellite Cells: Regenerative Mechanisms and Applicability in Muscular Dystrophy

Abstract

The satellite cells are long regarded as heterogeneous cell population, which is intimately linked to the processes of muscular recovery. The heterogeneous cell population may be classified by specific markers. In spite of the significant amount of variation amongst the satellite cell populations, it seems that their activity is tightly bound to the paired box 7 transcription factor expression, which is, therefore, used as a canonical marker for these cells. Muscular dystrophic diseases, such as Duchenne muscular dystrophy, elicit severe tissue injuries leading those patients to display a very specific pattern of muscular recovery abnormalities. There have been works on the application of precursors cells as a therapeutic alternative for Duchenne muscular dystrophy and initial attempts have proven the cells inefficient; however later endeavours have proposed solutions for the experiments improving significantly the results. The presence of a range of satellite cells populations indicates the existence of specific cells with enhanced capability of muscular recovery in afflicted muscles.

Tracking stem cells with superparamagnetic iron oxide nanoparticles: perspectives and considerations

“…105,106 Similar to other striated muscles, the injured cell milieu generated by the damage dictates the tropism of resident progenitor and stem cells to the injury site, mediating a certain degree of self-recovery, [103][104][105][106][107] but since the adult cardiomyocytes are known to be in mitotic arrest, this limits the repair mechanism. 108,109 Thus, considering the low regeneration potential of the endogenous mechanisms attempts to stimulate regeneration by using exogenous stem cells seem plausible.…”

The ubiquitin ligase tripartite-motif-protein 32 is induced in Duchenne muscular dystrophy

“…Exhaustion of this regeneration potential ultimately leads to replacement of the skeletal muscle with adipose and fibrotic connective tissue. 57 TRIM32-related mechanisms of action in satellite cells in DMD and possibly in other muscular dystrophies are particularly intriguing as there are multiple experimental strategies aimed at enhancing the regeneration of skeletal muscle in these disorders.…”

Investigational treatments and therapeutic targets in Becker muscular dystrophy

“…In the early phase of DMD/BMD, increased breakdown of muscle fibers is compensated by regeneration of new muscle fibers from quiescent satellite cells [16]. However, the limited numbers of satellite cells leave the rampant muscle necrosis uncompensated as the disease progresses.…”