squeegee
Banned
- Reaction score
- 132
NF-?B is associated with a range of interesting mechanisms: "Aging is associated with NF-?B-dependent pro-inflammation. Here we demonstrated that inhibition of NF-?B with pyrrolidine dithiocarbamate increases the median lifespan (13-20%) and the age of 90% mortality (11-14%) in Drosophila melanogaster females and males, respectively. ... NF-?B controls the expression of genes involved in innate immunity, inflammation and apoptosis. Such age-dependent pathologies as tissue inflammation and atrophy are caused by over-activation of the NF-?B signaling with age. ... Recent studies suggest that the NF-?B transcription factor controls age-dependent changes in inflammation genes expression. Donato et al showed that an increase of NF-?B dependent genes in human endothelium with age is primarily linked to [decreased] NF-?B inhibition. Age-associated expression of NF-?B-dependent genes cause progression of atherosclerosis in rat. Furthermore, selective inhibition of NF-?B activity in blood vessel endothelial cells prevents atherosclerosis progression. Genetic blockade of NF-?B in the skin of chronologically aged mice reverses the global gene expression program and tissue characteristics to those of young mice ... However, the effect of NF-?B inhibition on the lifespan was not studied before."
Merely this example "Genetic blockade of NF-?B in the skin of chronologically aged mice reverses the global gene expression program and tissue characteristics to those of young mice" is a very very interesting and possibly a significant "clue"... Certain genes start "drifting" from the optimal state due to lack of pressure from a natural selection, a cellular mess begins, you restore some of that to it's former state - voila, tissue goes back to "young". That's a great proof of the regulation of gene expression relation to the "aging state" of a tissue, and quite probably - a whole organism (I'm not educated enough to speculate how possible it would be to affect a whole epigenome of a mice and "bring it back" to the one it was when a mice was young, if that's possible at all, but I'd bet that would translate in the same effect - overall "age reversal".)..
Key words - "Gene expression program".
Merely this example "Genetic blockade of NF-?B in the skin of chronologically aged mice reverses the global gene expression program and tissue characteristics to those of young mice" is a very very interesting and possibly a significant "clue"... Certain genes start "drifting" from the optimal state due to lack of pressure from a natural selection, a cellular mess begins, you restore some of that to it's former state - voila, tissue goes back to "young". That's a great proof of the regulation of gene expression relation to the "aging state" of a tissue, and quite probably - a whole organism (I'm not educated enough to speculate how possible it would be to affect a whole epigenome of a mice and "bring it back" to the one it was when a mice was young, if that's possible at all, but I'd bet that would translate in the same effect - overall "age reversal".)..
Key words - "Gene expression program".