Senescence-driven disruption of monocyte identity in aging humans
As we age, our body is progressively less capable of dealing with stresses such as infection and physical damage, which leads to morbidity and disease. This decrease in systemic function is linked to a process called senescence, which drives cells into a dysfunctional state that promotes inflammation. Senescent cells accumulate in tissues as we age. Although we do not fully understand why senescent cells accumulate, there is increasing evidence that aging also impairs the function of the immune system, including its ability to remove damaged cells from tissues. Monocytes, one of the immune cell types, remove damaged cells and mediate immune responses. Emerging evidence shows that monocyte function is impaired with age, suggesting that these cells may undergo senescence with aging. Building on our previous work on manipulating gene regulatory networks of senescence, here we propose a multidisciplinary approach to characterize and modulate monocyte senescence.
