Fundamental Cell-Intrinsic Mechanism Underlying Age-Dependent Accumulation Of Senescent Cells
As we get older, our bodies accumulate “senescent cells” – cells that have stopped dividing but remain in tissues, often releasing harmful substances. These cells are known to contribute to various age-related diseases. Traditionally, scientists believed this accumulation was mainly due to our immune system becoming less efficient at clearing these cells, or because senescent cells themselves live longer or encourage neighboring cells to become senescent.
However, new research suggests an additional, fundamental reason: the cells themselves change with age, making them more susceptible to becoming senescent in the first place. This means that as a cell ages, internal “epigenetic” and “molecular” changes occur. Epigenetic changes are like modifications to the instruction manual (DNA) that tell a cell what to do, without changing the actual genetic code. These changes create an environment within the cell that makes it easier for the senescence program to activate.
This finding has significant implications for how we approach aging and age-related diseases. It suggests that simply removing senescent cells might not be enough to substantially slow down aging. Instead, strategies that target these upstream drivers of cellular dysfunction, such as age-associated epigenetic alterations, could be more effective. Essentially, “epigenetic rejuvenation” – reversing some of these age-related changes to the cell’s instruction manual – might help cells become more resilient to stress and reduce the rate at which they become senescent.
Source: link to paper