ITGB3 protein regulates cellular senescence, study finds


Cellular senescence is the point at which cells in the body cease to divide. It is a fundamental mechanism that helps control cellular lifespan and prevents the propagation of damaged cells. Prior studies have suggested cellular senescence as a potential contributor to aging and age-related disease, making it an attractive target for drug development. But how senescence is regulated is not well characterized.

Now a new study appearing in Cell Reports provides new clues to cellular senescence. The study, led by researchers from the Queen Mary University of London, Icahn School of Medicine at Mount Sinai, and The Francis Crick Institute, shows that a protein called integrin beta 3 (ITGB3) regulates senescence. This is the first time that ITGB3 has been implicated in cellular senescence.

A human body is made of trillions of cells, which must coordinate their actions for the body to function properly. A group of senescent cells has been found in tissues from old patients and at the initial stages of cancer. These cells lose the ability to proliferate, which has a potential effect on tissue function, but can communicate with nearby cells via the release of inflammatory proteins.

In the present study, the team used human primary fibroblasts and fibroblast cells donated by individuals to investigate cellular senescence. Their main findings included that the expression of ITGB3 accelerates the onset of senescence by activating TGF-β and ITGB3 is regulated by the Polycomb protein CBX7.

The researchers also found that cilengitide, a drug against ITGB3, is able to block senescence-related inflammation without affecting proliferation. Finally, they observed an increase in ITGB3 levels in certain tissues from mice. In summary, the results suggest ITGB3 as a regulator of cellular senescence. According to senior author Ana O'Loghlen, ITGB3 may be a therapeutic target for aging and early cancer.
 
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