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Age-associated alterations in murine dermis through inflammatory response with mitochondrial DNA deletions.


Maximus Peto’s Commentary

This group reports on some age-related changes in mouse skin which suggest potential involvement of the mtDNA common deletion and cellular senescence.


Age-associated alterations in murine dermis through inflammatory response with mitochondrial DNA deletions.
Geriatr Gerontol Int. 2019 May;19(5):451-457.
Kawaguchi K, Kim SE, Sugiyama D, Sugimoto M, Maruyama M
DOI: 10.1111/ggi.13635
PubMed publication date (edat): 3/2/2019

Abstract

AIM:
Skin aging is caused by intrinsic and extrinsic mechanisms. Because it is difficult to distinguish intrinsic mechanisms from extrinsic skin aging, the mechanisms of intrinsic skin aging remain unclear. The present study aimed to characterize age-associated alterations in murine skin and investigate the mechanisms of intrinsic skin aging.

METHODS:
We measured morphological changes in dorsal skin from young (aged 2 months) and old (aged 22-24 months) mice by histological analysis. Age-associated alteration of gene expression patterns was determined by quantitative polymerase chain reaction and immunohistochemistry. Reactive oxygen species production in mouse dorsal skin was detected by confocal laser scanning microscopy. Mitochondrial DNA deletions were detected by conventional polymerase chain reaction and quantitative polymerase chain reaction analyses.

RESULTS:
Chronologically aged skin had dermal atrophy caused by increased matrix-degrading enzymes and decreased collagen synthesis. Chronologically aged skin samples also had increased senescence-associated secretory phenotype factors, elevated reactive oxygen species production and a higher frequency of the mitochondrial DNA common deletion.

CONCLUSIONS:
These observations suggest that chronological skin aging is associated with increased frequency of the mitochondrial DNA common deletion and chronic inflammation through the reactive oxygen species-senescence-associated secretory phenotype axis.

PMID: 30821091
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Maximus Peto

Max Peto is a longevity researcher and founder of Long Life Labs. A biochemist by training, he studies the biochemistry of aging and longevity and has worked with research organizations such as SENS Research Foundation, Methuselah Foundation, BioAge Labs, Life Extension Foundation, and Ichor Therapeutics. His work at Long Life Labs is focused on empowering people to understand and manage the most critical factors for better health and longer life.

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