In lab-grown human fibroblasts, tiny vesicles from senescent cells prompted dividing cells to halt division and activate a DNA damage response.In lab-grown human fibroblasts, tiny vesicles from senescent cells prompted dividing cells to halt division and activate a DNA damage response.
In experiments in mice, blocking a protein-recycling pathway in immune cells increased the build-up of senescent cells, which had stopped dividing.In experiments in mice, blocking a protein-recycling pathway in immune cells increased the build-up of senescent cells, which had stopped dividing.
A drug screen in human connective-tissue cells linked the selective killing effect to a protein that receives growth signals.A drug screen in human connective-tissue cells linked the selective killing effect to a protein that receives growth signals.
In progeroid mice, activating the GPR81 receptor with the agonist CHBA reduced arterial lipid buildup, lowered cellular senescence, and improved endothelial integrity.In progeroid mice, activating the GPR81 receptor with the agonist CHBA reduced arterial lipid buildup, lowered cellular senescence, and improved endothelial integrity.