Abstract p16INK4a, located on chromosome 9p21. 3, is lost among a cluster of neighboring
tumor suppressor genes. Although it is classically known for its capacity to inhibit cyclin …

At first glance, cancer and ageing would seem to be unlikely bedfellows. Yet the origins for
this improbable union can actually be traced back to a sequence of tragic—and some say …

Several pharmacological, dietary, and genetic interventions that increase mammalian
lifespan are known, but general principles of lifespan extension remain unclear. Here, we …

Recent data suggest that we age, in part, because our self-renewing stem cells grow old as
a result of heritable intrinsic events, such as DNA damage, as well as extrinsic forces, such …

Expression of the p16INK4a tumor suppressor sharply increases with age in most
mammalian tissues, and contributes to an age‐induced functional decline of certain self …

One of the major conceptual advances in our understanding of the pathogenesis of age-
associated cardiovascular diseases has been the insight that age-related oxidative stress …

Expression of p16Ink4a and p19Arf increases with age in both rodent and human tissues.
However, whether these tumour suppressors are effectors of ageing remains unclear, mainly …

The rapid increase in both the lifespan and proportion of older adults is accompanied by the
unprecedented rise in age-associated chronic diseases, including sarcopenia and obesity …

Background Aging results in a progressive loss of skeletal muscle, a condition known as
sarcopenia. Mitochondrial DNA (mtDNA) mutations accumulate with aging in skeletal …

Cellular senescence is a state of cell cycle arrest induced by several forms of metabolic
stress. Senescent cells accumulate with advancing age and have a distinctive phenotype …