I exaggerate in the title of this post, of course, but there is some truth in it. Certainly, a lot more attention is focused on the phenomenon of cellular senescence now that mouse life spans have been extended and aspects of aging have been reversed via clearance of senescent cells. The existence of several startup biotechnology companies aiming to bring senescent cell clearance treatments to the clinic is shining even more of a spotlight on this area. It has been something of a transformation. Five years ago, one of the few groups of researchers interested in this field struggled greatly to raise the funding for the pivotal study to prove that selectively removing senescent cells had a significant impact on health. Five years from now, every major research center will have a cellular senescence arm in the same way that they have a cancer arm today. It is that important to that many aspects of aging and age-related disease.

Cells become senescent when they reach the end of their replicative life span, or in response to damage, or a toxic environment. They cease to divide, and largely destroy themselves or are destroyed by the immune system. It is an evolutionary adaptation that serves, at least initially, to suppress cancer by removing those cells most at risk of uncontrolled replication. Unfortunately not all are destroyed. Some remain, and their numbers grow over the years, secreting a disruptive mix of signal molecules that causes chronic inflammation, corrodes surrounding tissue structures, changes the behavior of healthy cells for the worse, and no doubt more that is yet to be cataloged. Recently researchers have shown that senescent cells contribute directly to the progression of atherosclerosis, as well as declining lung function and loss of tissue elasticity in that organ. The inflammation angle on its own is enough to link greater numbers of senescent cell to an increased risk of most age-related diseases, and a worse prognosis for long-term health. Then, of course, there is the life span study showing extended life in mice as a result of senescent cell clearance.

Senescent cell accumulation is only one of the processes that cause degenerative aging. Fixing it via periodic selective destruction of these cells is only a narrow, partial rejuvenation. There is still everything else in the SENS rejuvenation research agenda to work through. Nonetheless, it is a great improvement over the present state of medicine to have senescence cell clearance therapies on the horizon. Given that senescent cells can be linked to near every age-related condition via at least inflammatory mechanisms, and given the greatly increased awareness of cellular senescence in far-flung parts of the research community that probably weren't paying all that much attention in the past, we are now seeing the first of what will no doubt prove to be a wide selection of efforts to link preexisting theories, data, and viewpoints on aging and age-related disease to what is known of the biochemistry of cellular senescence. I offer the open access paper quoted below as one example of the type, though I wouldn't take everything the authors have to say about oxidative stress in aging at face value. They mention the supporting evidence, but omit the equally numerous counterexamples that demonstrate the relationship between oxidative damage and aging to be far from simple.

A new role for oxidative stress in aging: The accelerated aging phenotype in Sod1-/- mice is correlated to increased cellular senescence