Recent theories on aging focus around the concept that chronic inflammation may attribute to earlier mortality. One of my professors from the USC school of Gerontology put forward the theory that the extension of average lifespan seen in the last century is due to a decrease in lifelong inflammation starting at an early age, because of increases in sanitation and control of disease such as through vaccinations. Here is an article that finds a molecular clue to the connection between inflammation and aging through cancer. A small RNA molecule that is a marker for inflammation is found to down regulate another protein, Wee1, that signals the cell to stop the process of cell division when errors are present -preventing mutations and the chance of cancer:
Here is the actual research paper which shares these insights:
The control of cell-cycle progression and DNA repair in
eukaryotes are highly conserved. However, in the event of an
infection the cells must respond quickly by producing cytokines,
chemokines, and other inflammatory components of the immune
defense. During this robust response, it is possible that the DNA
repair machinery and cell-cycle checkpoints are put on hold. At
this stage the up-regulation of miR-155 by inflammatory stimuli
to clear the antigen quickly also results in an increased mutation
rate. Furthermore, regardless of the primary cause of a mutation,
there is a high probability that, in the event of an infection, the
mutation will be fixed. In conclusion, we believe that
simultaneous miR-155–driven suppression of a number of
tumor suppressor genes combined with a mutator phenotype
allows the shortening of the series of steps required for tumorigenesis and
represents a model for cancer pathogenesis.
"The investigators learned that miR-155 also targets WEE1 and showed that high levels of miR-155 lead to low levels of WEE1. They reasoned that low levels of WEE1 allowed cell division to continue even when DNA damage is present, leading to a growing number of mutations." | |
Here is the actual research paper which shares these insights:The control of cell-cycle progression and DNA repair in
eukaryotes are highly conserved. However, in the event of an
infection the cells must respond quickly by producing cytokines,
chemokines, and other inflammatory components of the immune
defense. During this robust response, it is possible that the DNA
repair machinery and cell-cycle checkpoints are put on hold. At
this stage the up-regulation of miR-155 by inflammatory stimuli
to clear the antigen quickly also results in an increased mutation
rate. Furthermore, regardless of the primary cause of a mutation,
there is a high probability that, in the event of an infection, the
mutation will be fixed. In conclusion, we believe that
simultaneous miR-155–driven suppression of a number of
tumor suppressor genes combined with a mutator phenotype
allows the shortening of the series of steps required for tumorigenesis and
represents a model for cancer pathogenesis.
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