There are two models of premature aging; progeria and trisomy 21.
What protects rapidly aging cells protects our shower aging cells.
Nrf2 slows aging and cell senescence in trisomy 21.
Nrf2 slows aging in every cell.
Therefore Nrf2 is one target of the coin of RESILIENCE.
The flip side is reducing autoimmunity that results from inflamaging.
Tails is increasing Vagal tone and activating the cholinergic anti inflammatory pathway via slow paced breathing with or without augmentation by facial cooling.
RESILIENCE includes Nrf2 activation and autoimmunity deactivation.
Nrf2 stabilization prevents critical oxidative damage in Down syndrome cells - Zamponi - - Aging Cell - Wiley Online Library
Mounting evidence implicates chronic oxidative stress as a critical driver of the aging process. Down syndrome (DS) is characterized by a complex phenotype, including early senescence. DS cells display increased levels of reactive oxygen species (ROS) and mitochondrial structural and metabolic dysfunction, which are counterbalanced by sustained Nrf2‐mediated transcription of cellular antioxidant response elements (ARE). Here, we show that caspase 3/PKCδdependent activation of the Nrf2 pathway in DS and Dp16 (a mouse model of DS) cells is necessary to protect against chronic oxidative damage and to preserve cellular functionality. Mitochondria‐targeted catalase (mCAT) significantly reduced oxidative stress, restored mitochondrial structure and function, normalized replicative and wound healing capacity, and rendered the Nrf2‐mediated antioxidant response dispensable. These results highlight the critical role of Nrf2/ARE in the maintenance of DS cell homeostasis and validate mitochondrial‐specific interventions as a key aspect of antioxidant and antiaging therapies.
Joseph Thomas (Tony) Liverman, Jr.
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