The proof-reading defective mtDNA polymerase γ (POLG) mutant mouse strains that develop age-dependent cardiac hypertrophy are used as a model of aging, and it was shown using TEM that megamitochondria appear to be present in the POLG and the POLG:Parkin OE mice, whereas neither whole-body Parkin KO or cardiac Parkin OE rescued these POLG-dependent changes in mitochondrial morphology (Woodall et al., 2019). Here, PRKN is linked to cardiac hypertrophy.