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- W2419215047 abstract "The pathophysiological process of natural human aging has not been studied adequately due to the lack of an appropriate human model. Since recent investigations have suggested that possibly contributes to the pathogenesis of age-related disorders including atherosclerosis, cancer, and diabetes mellitus, the term inflammaging, a combination of inflammation and has been coined. Werner syndrome (WS), caused by the loss of function of RecQ3 DNA/RNA helicase, is a typical progeroid syndrome mimicking natural aging, although it is extremely rare outside of Japan. We sought to examine WS patients from an immunological/inflammatory perspective. Sera from 14 mutation-proven WS patients (ages: 33-70 years) and 21 healthy Japanese adults ages 15 to 95 years were examined with ELISA for soluble Fas ligand (sFasL) to compare conventional markers. With natural aging, a statistically significant correlation (p < 0.0001) was observed in the serum level of sFasL. The sFasL in WS, a level comparable to that in healthy elderly ages 83 to 95 years, had significantly increased (p < 0.05) compared to that in young healthy individuals ages 15 to 70 years. A significant correlation was noted between the serum levels of conventional markers such as CRP (p < 0.025), ESR (p < 0.024), and WBC count (p < 0.0085). In conclusion, an increased level of serum sFasL in natural aging and WS patients may suggest a common pathophysiological mechanism: inflammation. WS may be a good model for analyzing inflammaging." @default.
- W2419215047 created "2016-06-24" @default.
- W2419215047 creator A5091648023 @default.
- W2419215047 date "2008-06-01" @default.
- W2419215047 modified "2023-09-23" @default.
- W2419215047 title "Elevation of soluble Fas (APO-1, CD95) ligand in natural aging and Werner syndrome." @default.
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