New Senescence Signalling Mechanism Discovered

Credit: NIH

A member of the integrin family, integrin beta 3, is highly expressed in senescent cells and could be a new therapeutic target to ameliorate their harmful effects

Senescent cells are one of the most well characterized elements of the aging process, and removing them is likely to be one of the first real 'anti-aging' medical interventions we see come to market. These dysfunctional, old cells have ceased dividing and spread inflammatory, detrimental signals into their environment; driving bodywide inflammation, cancer risk and breaking down surrounding tissue. Finding new ways to block their effects and eradicate them is crucial. 

A new target

Using human fibroblast cells from young and old donors, a team from Queen Mary University of London has discovered an important way that these senescent cells communicate - via integrin membrane proteins. More specifically, these cells appear to enrich expression of a particular protein called integrin beta 3 which activates a pathway called TGFβ. The same protein appears to be upregulated in old mice tissue too, suggesting it's a conserved mechanism. Interestingly, there is already a drug that interferes with integrin beta 3, called Cilengitide. The researchers showed that blocking integrin beta 3 could avert the negative effects of the senescence-associated secretory phenotype (SASP). This makes it a promising new therapeutic target for future research. 

"This is the first time that integrin beta 3 has been identified in the context of senescence and ageing, and could be in the future a potential therapeutic target during early carcinogenesis and ageing. This finding is particularly interesting, as there is actually a drug against integrin beta 3, called 'cilengitide', that averts one of the disadvantages of ageing in our model - inflammation. It does this without increasing cell proliferation, which is an advantage, as an increase in cell proliferation imposes a risk for cancer"

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