Muscle regeneration ability depends on muscle stem cells marked with Pax; knowing as muscle satellite cells (MuSCs). But in adult skeletal muscle; including in myofibers Dlk1 expression is rarely detecting. Dlk1 expression is also detecting in adult murine regenerating muscle; suggesting that Dlk1 is an important factor for muscle regeneration or degeneration.
Using cardiotoxin injury model; muscle experiments revealed impaired regeneration processes; suggesting that muscle regeneration is limiting due to the loss of Dlk1 in Myf5-positive myogenic lineage cells. But mesenchymal progenitors, also knowing as the fibro/adipogenic progenitors, exhibiting adipogenic differentiation ability in both humans and rats.
Progenitors muscle regeneration
Because fat accumulation decreases skeletal muscle integrity, force, and function, numerous study have been conducted to evaluate the molecular mechanism underlying the adipogenic differentiation of mesenchymal progenitors. The accumulation of adipocytes and expression of Dlk1 in regenerating muscle suggests a correlation between fat accumulation and Dlk1 expression in the muscle.
Additionally, mice overexpressing Dlk1 show increased muscle weight; while Dlk1-null mice exhibit decreased body weight and muscle mass, indicating that Dlk1 is a critical factor in regulating skeletal muscle mass during development. The muscle regeneration process shares some features with muscle development.
Muscle stem cells
However, the role of Dlk1 in regeneration processes remains controversial. But deletion of Dlk1 in neither the muscle stem cells nor the mesenchymal progenitors; affecting the regenerative ability of skeletal muscle. In addition, fat accumulation was not increasing by the loss of Dlk1. Collectively; Dlk1 plays essential roles in muscle development; but does not greatly impact regeneration processes and adipogenic differentiation in adult skeletal muscle.
Mesenchymal progenitors are defining by their ability to differentiate into adipocytes; and ectopic adipocyte accumulation in the skeletal muscle is detected in patients with muscular dystrophy. In contrast, mesenchymal progenitors also promote the process of muscle.