Linking RAGE, DNA Damage, Cellular Senescence, and Reversible Fibrosis

Researchers here find that loss of RAGE in mice produces accelerated fibrosis that is reversible if RAGE is restored. It is a little early in this line of research to be enthused by it; I think that all that is being shown here is that fibrosis is principle reversible, though this is interesting enough to merit comment in and of itself. It is frequently the case that a form of accelerated disease progression has little relevance to the biochemistry of the real thing. Acceleration usually takes the form of one aspect of the disease progress being exaggerated out of proportion, and that aspect may well not play a significant role in comparison to the other aspects of its biochemistry. This research is also of interest because RAGE, the receptor for advanced glycation end-products (AGEs), is implicated in age-related inflammation. AGEs come in a variety of types, and readers here are probably more familiar with the persistent glucosepane AGEs that form cross-links in tissue, damaging structural properties and function. There are a whole range of other types of AGEs that are more transient, more dependent on diet, and which cause issues via their interaction with RAGE. The better known activities of RAGE are unrelated to the focus in this paper, however. Like many proteins, RAGE has more than one job, and those jobs have little relation to one another. Of relevance here, RAGE is vital to DNA repair, and so loss of RAGE produces greater levels of cell dysfunction and...
Source: Fight Aging! - Category: Research Authors: Tags: Daily News Source Type: blogs