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I have no idea. All I can say is that the paper overwhelmingly uses the term "senolytic", which means to "kill off the senescent" (I'm assuming that it refers to senescent cells), as opposed to "senostatic", which means to "delay senescence". Additionally, the concern brought up by the paper, is that senescent cells are known to be resistant against something called "apoptosis", which is a term to describe "programmed cell death". The goal of the paper is to explore a compound—fisetin—for its senolytic capabilities. Whether it is successful at finding that, I haven't fully read the paper to see if they have identified fisetin as a senolytic, or a senostatic agent. With that said, however, some of the graphs in the paper does highlight that as fisetin dose increases, not only do senescent cells get depleted, but so do total number of cells. If we were working with a purely senostatic agent, relative to a control, the senescent cells would be much lower, but the overall cell count would be much higher, which is not the case with fisetin. Does this mean that fisetin is a senolytic? Maybe not; it could just indiscriminately target all cells, resulting in fewer cells. Or maybe it is. Who knows. Or maybe my logic about cell counts regarding senostatic vs senolytic may be entirely wrong. Whatever it is, I haven't read the whole paper. |