Abstract:
:The gerosuppressant metformin operates as an efficient inhibitor of the mTOR/S6K1 gerogenic pathway due to its ability to ultimately activate the energy-sensor AMPK. If an aging-related decline in the AMPK sensitivity to cellular stress is a crucial event for mTOR-driven aging and aging-related diseases, including cancer, unraveling new proximal causes through which AMPK activation endows its gerosuppressive effects may offer not only a better understanding of metformin function but also the likely possibility of repositioning our existing gerosuppressant drugs. Here we provide our perspective on recent findings suggesting that de novo biosynthesis of purine nucleotides, which is based on the metabolism of one-carbon compounds, is a new target for metformin's actions at the crossroads of aging and cancer.
journal_name
Aging (Albany NY)journal_title
Agingauthors
Menendez JA,Joven Jdoi
10.18632/aging.100523subject
Has Abstractpub_date
2012-12-01 00:00:00pages
894-8issue
12issn
1945-4589pii
100523journal_volume
4pub_type
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