Mitochondria in the Aging Muscles of Flies and Mice: New Perspectives for Old Characters

Table 1

Summary of the evidence for mitochondrial homeostatic mechanisms altered during aging of flies compared to mice.

		Mice		Flies
Oxidative stress		ROS [15]; Affects the complex V (ATP synthase) of the ETC [21]		ROS [22, 35]
Antioxidant systems		Diminished ROS scavengers’ activity during aging [33]; Overexpression of human mitochondrial catalase in old mice protects from oxidative damage and age-associated mitochondrial dysfunction [36]		Diminished ROS scavengers’ activity during aging [32, 34]; Genetic manipulation of catalase and superoxide dismutase protein, SOD, could alter lifespan in the fly [32, 34]
mtDNA		Increase of 8-oxodeoxiguanosine (8-oxoG), indicating mtDNA oxidation; Alteration of mtDNA copy number in muscle cells [24, 29, 30].; mtDNA haplotype mutation arise in early life [26]		Naturally occurring variations in mtDNA influence mitochondrial bioenergetics [22, 23]; Alteration of mtDNA copy number in muscle cells [22, 23]; mtDNA haplotypes may correlate with lifespan [23]
Mitochondrial dynamics		Enlarged mitochondria in aging muscles; Mitochondrial fusion/fission genes show altered expression in old animals [39]		Drp1 mutants harbor fewer mitochondria at the neuromuscular junction [40]; Drp1 muscle knockdown shows alterations in mitochondrial morphology and distribution [41, 42]
Ca^2+ regulation		Impaired EC-coupling [43].; Reduced supply of Ca^2+ ions to the contractile elements; Age-dependent uncoupling of mitochondria from the Ca^2+ release units [43–46]		Heart tubes deficient of MARF (dMFN) had increased contraction-associated and caffeine-sensitive Ca^2+ release, suggesting a role for MARF in SR Ca^2+ handling [47].

ETC: Electron Transport Chain; ROS: Reactive Oxygen Species; EC: Excitation-Contraction coupling; mtDNA: mitocondrial DNA; Drp1: Dynamin-related protein 1; MARF: Mitochondrial Assembly Regulatory Factor; dMFN: Drosophila Mitofusin; SR: Sarcoplasmic Reticulum.