As we age, our bodies become more fragile, a change linked to the accumulation of cells that have stopped dividing. Sometimes nicknamed "zombies," these cells that are still alive but non-functional fuel inflammation and the development of chronic diseases.
These senescent cells persist in tissues and release inflammatory molecules, a phenomenon called the senescence-associated secretory phenotype. This process contributes to age-related decline. Although the body normally has a system to eliminate them, this function loses efficiency over time, promoting their accumulation.
To understand their persistence, researchers at Kyoto University focused on a key energy process, glycolysis, also used by cancer cells. Their attention turned to two molecules, phosphoglycerate mutase and Chk1 kinase. Their bond appears strengthened in senescent cells, an interaction that maintains their energy production and cellular survival, as laboratory tests have shown.
Using a bioluminescence detection technique, the team was able to observe these protein bonds. Blocking this connection leads to the selective elimination of senescent cells, both in culture and in mice. This manipulation also alleviated pulmonary fibrosis in the rodents, hinting at potential health benefits.
This blockage also acts on a central mechanism in the cell cycle. By reducing its activity, damaged cells can enter apoptosis, programmed cell death. This is akin to self-elimination.
Published in
Signal Transduction and Targeted Therapy, this work shows that it might be possible to restore to the body capabilities lost with aging.