Fig. 8: Rrm2b deletion in the myofibers promotes differentiation and arrests quiescence of stem cells when skeletal muscle is injured.
From: Ribonucleotide reductase M2B in the myofibers modulates stem cell fate in skeletal muscle
a Under muscle damage, quiescent MuSCs enter the cell cycle, proliferate, and are then activated. Activated MuSCs either differentiate to form new myofibers or self-renew to re-enter the quiescent stage. b In the Rrm2b knockout myofibers, increased myokines continuously drive spontaneous MuSC activation and differentiation but inhibit self-renewal, resulting in a low number of MuSCs and myofiber weakness. c Our working hypothesis revealed that Atf4 and Errγ through PGC1α-independent signaling pathways and mitochondrial defects, upregulated expressions of Fgf21, Gdf15, Mthfd2 and other factors, which associated myogenesis in the Rrm2b-deleted myofibers.
