Key points from article :
Age-related dysfunctions often termed the 'hallmarks of aging' are approached as distinct mechanisms.
Hallmarks are not discrete entities but are interconnected and overlapping.
Identification of links between NAD+ decline, cellular senescence, and chronic inflammation.
NAD+ plays a key role in biological processes, ranging from energy metabolism to cell survival and repair.
Cellular senescence prevent unrestricted division of damaged and potentially cancerous cells.
Restoration of NAD+ and selective elimination of senescent cells extend lifespan.
Falling NAD+ levels and senescent cell recruitment are mediated via chronic inflammation.
Accumulation of senescent cells with age leads to increased pro-inflammatory SASP.
SASP leads to CD38 expression and concurrent decrease in NAD+ levels.
CD38 inhibitor 78c reverse age-related NAD+ decline and improve physiological and metabolic parameters of aging.
Several factors must be addressed at once, targeting the cascading network of age-related decline.
