Fig. 2
From: RETRACTED ARTICLE:Exercise-induced mitochondrial p53 repairs mtDNA mutations in mutator mice
Endurance exercise prevents dysregulated mitochondrial-induced apoptosis, reduces nuclear p53-mediated repression of PGC-1α, induces PGC-1α regulated gene networks, restores mtDNA copy number, and normalizes mitochondrial morphology in mtDNA mutator mice. a Nuclear DNA fragmentation (apoptotic index) in the heart, HSC, and SC of WT, PolG-SED, and PolG-END (n = 7–10/group). b ChIP assay showing reduced p53 enrichment of PGC-1α promoter (positions −954/−564) with exercise in the muscle and heart of WT, PolG-SED, and PolG-END (n = 6/group). c Gene expression of PGC-1α and its downstream targets in muscle (quadriceps femoris), d mtDNA copy number normalized to nuclear β-globin gene in the muscle (soleus) and heart, and e representative electron micrographs of myofibers (quadriceps femoris) and cardiomyocytes (heart) from WT, PolG-SED, and PolG-END mice (n = 4–7/group). Asterisk (PolG-SED vs. both WT and PolG-END): *P < 0.05, **P < 0.01, ***P < 0.001. Error bars represent SEM. AU arbitrary units