A recent open access review paper looks at the evidence for accumulated senescent cells as one of the causes of aging: "Epidemiological studies have shown that age is the chief risk factor for lifestyle-related diseases such as cardiovascular disease and diabetes, but the molecular mechanisms that underlie the increase in the risk of such diseases conferred by aging remain unclear. ... Interestingly, most of the molecules that influence the phenotypic changes of aging also regulate cellular senescence, suggesting a causative link between cellular senescence and aging. ... Cell division is essential for the survival of multicellular organisms that contain renewable tissues, but places the organism at risk of developing cancer. Thus, complex organisms have evolved at least two cellular mechanisms to prevent [cancer]: apoptosis and cellular senescence. In this regard, aging and age-associated diseases can be viewed as byproducts of the tumor suppressor mechanism known as cellular senescence. Consistent with this idea, the number of senescent fibroblasts increases exponentially in the skin of aging primates. Conversely, extension of the lifespan by calorie restriction decreases biomarkers of cellular senescence."