What will happen to molecular and cellular biomarkers of aging in case its program is canceled (provided such a program does exist)?

Today, gerontologists usually employ certain molecular or cellular biomarkers of aging to evaluate the effects of various interventions in this process, since this approach is much more time-efficient than the construction of survival curves. However, arguments for the expediency of using such biomarkers are often based on the results of studies on what is called cell/cellular senescence. Unfortunately, the usage of this term has recently evolved so that it has largely lost its initial meaning, which is that normal cultured cells are subject to replicative senescence (according to the Hayflick phenomenon) and undergo changes similar to those in the cells of an aging organism. Most of recent studies in this field deal with the induction of relevant changes in cultured (usually transformed) cells by various DNA-damaging factors. Such an approach is important for defining the strategy of cancer control but, yet again, leads away from the study of actual mechanisms of organismal aging. Moreover, there are grounds to consider that biomarkers of aging identified in these studies (in particular, senescence-associated beta-galactosidase activity, the most popular among them) are basically linked to cell proliferative status. At the organismal level, this status is generally determined by the program of development and differentiation of tissues and organs, which in a definitive state are composed of postmitotic or very slowly propagating cells. Therefore, it appears that canceling the aging program will not cause any significant changes in the age-dependent dynamics of the above biomarkers. This conclusion brings us back to the necessity of constructing the survival curves for test groups of animals or humans as the only reliable (though expensive and time-inefficient) approach to evaluating the efficiency of means to modify the aging process.