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Reduced expression of mitochondrial complex I subunit Ndufs2 does not impact healthspan in mice

ABSTRACT: Aging in mammals leads to reduction in genes encoding the 45-subunit mitochondrial electron transport chain (ETC) complex I. It has been hypothesized that normal aging and age-related diseases such as Parkinson’s disease are in part due to modest decrease in expression of mitochondrial complex I subunits. By contrast, diminishing expression of mitochondrial complex I genes in lower organisms increases lifespan. Furthermore, metformin, a putative complex I inhibitor increases healthspan in mice and humans. In the present study, we investigated whether loss of one allele of Ndufs2, the catalytic subunit of mitochondrial complex I, impacts healthspan and lifespan in mice. Our results indicate that Ndufs2 hemizygous mice (Ndufs2+/-) show no overt impairment in motor function, learning, tissue histology, organismal metabolism, or sensitivity to metformin in a C57B6/J background. However, there are detectable changes at the level of gene expression in individual cell types and tissues due to loss of one allele of Ndufs2. Our data indicate that modest decline in expression of mitochondrial complex I subunit Ndufs2 is not detrimental to healthspan.

ORGANISM(S): Mus musculus

PROVIDER: GSE190689 | GEO | 2021/12/12

REPOSITORIES: GEO

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