Therapies for senescent cell clearance as a treatment for aging are going to be an ongoing concern within the next few years. Multiple different methods have been demonstrated to selectively kill senescent cells in mice, including the genetic engineering approach used a few years ago and the various senolytic drug candidates discovered more recently. These have variable effectiveness in different tissues, with some tissue types retaining all of their senescent cells, suggesting that no initial clinical treatment is going to be perfect. Even these prototypes are, however, clearing as much as a quarter of senescent cells in some tissues. In the case of senolytic drugs this is enough for old mice to display lasting health benefits after even a single treatment.
Why is the destruction of senescent cells an important goal? In short because cellular senescence is a contributing cause of aging. When damaged or faced with a toxic, stressed environment, cells tend to become senescent. A senescent cell stops replicating and secretes signals that both adjust the behavior of surrounding cells, making them more likely to become senescent, and make the senescent cell itself a target for destruction by the immune system. This is probably a defense against cancer, removing from play those cells most likely to become cancerous. Evolution likes reuse, and senescent cells are also transiently involved in wound healing and structural control over embryonic development. Nonetheless, having too many senescent cells is a bad thing, and that is exactly what happens with advancing age: senescent cells that evade destruction linger indefinitely, and their numbers grow over time, especially once the immune system starts to decline in old age. In large numbers senescent cells cause chronic inflammation and their collective signaling actively harms tissue structure and function. Their presence contributes to all of the common age-related diseases via these and a range of other, similar mechanisms. Periodic removal of senescent cells would solve all of these problems.
Senescent cell clearance treatments could be made much more efficient than the prototypes demonstrated so far in mice. That seems inevitable, based on some combination of innovation in delivery methods and innovation in kill mechanisms. We should always expect the first approaches to be weak in comparison to those that come later, with the benefit of more funding and attention. It is, however, quite possible for a therapy to be too good at killing senescent cells. Consider the study from some years back that showed as many as 20% of the skin cells in old baboons exhibited the signature for senescence. Now, what do you imagine would happen to you if 20% of the cells throughout your body died in a matter of a day? It wouldn't be pleasant. Clearing cells isn't a magical clean sweep of a process: a dead cell leaves behind debris and lot of frantic signaling in its last moments, and in volume that can be far worse than just leaving the cells alone. This is a well known problem in the cancer research community, a section of the medical establishment very focused on selectively killing cells. The condition that can result from having a significant number of cells die in a short period of time as the result of treatment is known as tumor lysis syndrome. At the mild end of the spectrum the outcome is sickness and metabolic dysregulation, while severe cases bring kidney failure and death, the systems of blood filtration utterly overwhelmed by a flood of cell debris and toxins.
Thus, naively, a hypothetical highly efficient senescent cell clearance therapy might work just fine in a 40-something adult, with tissues containing comparatively few senescent cells, while having a strong chance of killing patients in their 70s, with tissues containing many more senescent cells and also possessed of less resilient organs. Fortunately this issue is well understood in the research community, so no such highly efficient therapy is ever going to be produced. Approaches that could be this efficient in theory will be diluted or otherwise limited and delivered over a number of spaced treatments, producing a steady or stepped destruction of senescent cells at a safe pace. What that safe pace will turn out to be in humans is an open question, to be answered by experimentation, trials, and further studies, but the mouse data suggests it can be fairly rapid - just not all at once, immediately.