Mito
Member
- Joined
- Dec 10, 2016
- Messages
- 2,554
“Accumulating evidence suggests a strong link between mitochondrial dysfunction, mitochondrial diseases, aging, and aging-associated diseases26, 28, 30, 38, 63. Notably, increased somatic mtDNA mutations and decline in mitochondrial functions have been extensively reported during human aging26, 28, 30. Studies also suggest a decrease in mtDNA content and mitochondrial number with age32, 33, 64. The major finding of our study is that the ubiquitous depletion of mtDNA predominantly leads to wrinkled skin and hair loss accompanied by inflammatory phenotype. Wrinkled skin and hair loss are obvious features of skin aging and aging-associated phenotypic changes in humans. We discovered that these aging-associated phenotypic changes could be reversed by restoring mtDNA content to wild-type level. To our knowledge this observation is unprecedented.”
"......These experiments show that mitochondria are regulators of skin aging and loss of hair. This observation is surprising and suggests that epigenetic mechanisms underlying mitochondria-to-nucleus cross-talk must play an important role in the restoration of normal skin and hair phenotype.....”
https://www.nature.com/articles/s41419-018-0765-9
"......These experiments show that mitochondria are regulators of skin aging and loss of hair. This observation is surprising and suggests that epigenetic mechanisms underlying mitochondria-to-nucleus cross-talk must play an important role in the restoration of normal skin and hair phenotype.....”
https://www.nature.com/articles/s41419-018-0765-9