Abstract
Mitochondrial DNA (mtDNA) mutations accumulate in somatic stem cells during ageing and cause mitochondrial dysfunction. In this review, we summarize the studies that link mtDNA mutations to stem cell ageing. We discuss the age-related behaviours of the somatic mtDNA mutations in stem cell populations and how they potentially contribute to stem cell ageing by altering mitochondrial properties in humans and in mtDNA-mutator mice. We also draw attention to the diverse fates of the mtDNA mutations with different origins during ageing, with potential selective pressures on the germline inherited but not the somatic mtDNA mutations.
Highlights
Ageing is a process where tissue gradually loses homeostasis and regeneration [1]
These findings provide evidence that links the accumulation of somatic Mitochondrial DNA (mtDNA) mutations to stem cell ageing
We have provided evidence of the somatic mtDNA mutations accumulating in stem cell populations in normal humans and discussed their tissue-specific ability to expand clonally during ageing
Summary
Ageing is a process where tissue gradually loses homeostasis and regeneration [1] This process is systemic and closely associated to age-related changes in somatic stem cells [2]. These cells renew themselves and differentiate into tissue-specific daughter cells for tissue maintenance and regeneration. The age-related alterations in somatic stem cell properties include failure to generate functional progenies, depletion of the stem cell pool and cancerous transformation [3] These changes largely affect mitotic tissue, such as blood, intestine and skin, where the stem cells actively produce progenies to maintain the high turnover of the tissue [4,5]. We want to draw attention to an intriguing age-related phenomenon of the germline inherited mtDNA mutations in patients with mitochondrial disorders, as opposed to the accumulated somatic mtDNA mutations in normal individuals, as mtDNA mutations from different origins seem to have diverse fates with age
Sign-in/Register to view highlights & summary 
Published Version (
Free)
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call