Arguing for Cellular Senescence to be Significant in the Development of Osteoarthritis

There are two ways to provide evidence for a specific cellular mechanism to cause a specific age-related disease. The first, the better method, is to remove, block, or work around the mechanism, while changing as few other variables as possible. This is better because it can lead immediately to the development of a therapy if it turns out that the mechanism in question is important. The worse option is to make the mechanism more active, while changing as few other variables as possible, and see if problems happen more rapidly because of that alteration. This is worse because there is always the risk that greater activity in any biological process does cause greater harm, but is nonetheless not actually relevant to aging and age-related disease because that greater activity never happens in the normal course of matters. DNA repair deficiency is a great example of the type. Significant impairment of DNA repair produces damage, dysfunction, and accelerated disease and mortality, but really isn't all that relevant to normal aging. All that this tells us is that it is important that DNA repair functions correctly, in the same way that it is important to breathe, or important that hearts beat and blood flows. There are many ways to cause damage by breaking the operation of our biochemistry - you can hit living organisms with a hammer, for example - but very few of them tell us much about aging and age-related disease. With that preamble out of the way, today I'll point you t...
Source: Fight Aging! - Category: Research Authors: Tags: Medicine, Biotech, Research Source Type: blogs