As Chris Patil points out, the latest Annals of the New York Academy of Sciences contains a number of interesting papers. The two that jump out at me today relate to the aging of stem cells, a topic I've touched on before. How and why do the capacities of stem cells to repair your tissue deteriorate with age, and what can medical research do about this degeneration in the near term? These papers are modest components in the larger picture: progress towards answers, and from answers to interventions.
A decline in adult stem cell function occurs during aging, likely contributing to the decline in organ homeostasis and regeneration with age. An emerging field in aging research is to analyze molecular pathways limiting adult stem cell function in response to macromolecular damage accumulation during aging. Current data suggest that the p21 cell cycle inhibitor has a dual role in stem cell aging: On one hand, p21 protects adult stem cells from acute genotoxic stress by preventing inappropriate cycling of acutely damaged stem cells. On the other hand, p21 activation impairs stem cell function and survival of aging telomere dysfunctional mice indicating that p21 checkpoint function is disadvantageous in the context of chronic and persistent damage, which accumulates during aging. This article focuses on these dual roles of p21 in aging stem cells.
This is essentially cancer versus aging, as is often the case in regulatory functions related to the cell life cycle. Do you want damaged stem cells churning away, raising the risk of the biochemical accidents that generate cancer, or do you want to damp down the repair function, thereby accumulating more damage that causes aging? No good choice there, but the future of medical science provides other approaches - such as repairing the damage via new technologies.
In humans aging is a complex process that determines many physical and metabolic alterations correlated to the accumulation of oxidative damage in different tissues. Sarcopenia is an age-related nonpathological condition that includes a progressive loss of mass and strength in skeletal muscle, associated with a decline in the fibers' functional capability. This condition could be correlated to abnormal reactive oxygen species (ROS) accumulation with consequent fiber oxidative damage. This complex situation is not only evident in mature muscle fibers but also in muscle resident satellite cells (involved in fiber damage repairing)
These results suggest that during donor's life the satellite cells undergo an aging process similar to the one observed in skeletal muscle tissue, even if they are in a quiescence status for most of the time.
The failing capabilities of satellite cells in muscle have come up before here at Fight Aging! For example:
- More On Myostatin and Satellite Cells in the Aging Body
- Rejuvenating Aging Stem Cells ... Or Not
- Old Cells, Young Environment
One small part of the whole, but it shows just how rapid, broad and deep the river of science runs. Even in the just the past few years, understanding has advanced in leaps and bounds. Where next? That's up to us.