Senescent Cells Promote Wound Healing

Senescent cells stop dividing and secrete various factors that, among other things, damage surrounding tissue structure and encourage senesence in nearby cells. It would be best if they were removed, and they often are, either through programmed cell death or destroyed by the immune system. Some always remain however, and remain for the long term: their accumulation is one of the causes of degenerative aging. Senescence has some positive roles, however: when it occurs in response to a damaged tissue environment that leads to a greater risk of cells becoming cancerous then senescence can help reduce those odds by removing the cells most at risk from active duty. In addition senescence appears to be a necessary part of shaping tissue during embryonic growth.

Current investigations of senescence have turned up another beneficial role: some of the molecules secreted by senescent cells are a part of the processes of wound healing. Fortunately this is no obstacle to the future production of therapies to periodically clear senescent cells from the body, and thus remove this contribution to the aging process. Just don't use the treatments when you happen to be injured.

[Researchers] identified a single factor secreted by senescent cells that cause them to promote wound healing. It's a crucial discovery for researchers who are working on developing treatments to clear the body of senescent cells as a way to stem the development of age-related disease. "We are now able to identify what senescent cells express that makes them beneficial. This means we will be able to simply provide that factor while we eliminate senescent cells to prevent a deleterious side effect before it even occurs."

[Researchers] used two different mouse models: in the first, senescent cells can be visualized and eliminated in living animals; in the second, mutations in two key genes block the senescence program. Following a skin wound, senescence occurs early on in cells that produce collagen and line blood vessels. The senescent cells accelerated wound closure through the secretion of PDGF-AA, a growth factor contained within blood platelets, making it the "good guy" in this portrayal of senescence. "We were able to apply recombinant PDGF-AA topically to mice that had senescent-free wounds. It rescued delayed wound closure and allowed the mice to heal normally."

The researchers also found that senescent cells were present only for a short time during tissue repair, in contrast to the persistent presence of senescent cells in aged or chronically damaged tissues. Moreover, they say the fact that PDGF-AA was activated very early upon senescence induction in cell culture suggests the time-dependent regulation of secretory factors might, in part, explain the beneficial vs. deleterious effects of senescent cells. The possibility of eliminating senescent cells holds great promise and is one of the most exciting avenues currently being explored in efforts to extend healthspan. This study shows that we can likely harness the positive aspects of senescence to ensure that future treatments truly do no harm."


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