Inflammatory signaling disrupts all sorts of normal tissue functions. In the short term this is usually beneficial; inflammation is a necessary part of wound healing, defense against pathogens, and even destruction of errant cells. It is required to mobilize the immune system and coordinate the activities of various classes of immune cell with those of other cell populations. Unfortunately inflammation becomes chronic in later life, and the constant inflammatory signaling – and cellular reactions to that signaling – degrades normal function and produces lasting damage as a result. This particularly noteworthy when it comes to loss of regenerative capacity and generation of harmful fibrosis.
Chronic inflammation in aging and disease has long been a topic of interest for the research community, and a great deal of effort has been put into trying to understand the fine details of inflammation and means to control it. The newfound acceptance of the past few years that accumulation of senescent cells and growth in their potent inflammatory signaling is a significant cause of degenerative aging has only reinforced this part of the field.
“Inflammatory signaling” is, however, a very broad category. The processes of inflammation are
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