I found a free review that has collected and reviewed most methods of rejuvenating somatic stem cells attempted so far.
The results shouldn't be anything new to anyone on these forums but could prove to be interesting reading for newcomers.
http://www.ncbi.nlm....les/PMC4160113/
Conclusion
Stem cell aging is affected by many different cell-intrinsic and cell-extrinsic pathways, which often show cross-talk in the determination of stem cell function. This interdependence makes it difficult to place particular weight on any one pathway with respect to aging mechanisms; however, certain signals do appear more broadly involved than others, at least given available data, and this could imply that they are more important regulators of aging stem cells. For example, the mTOR pathway has been shown to be a major regulator of both ROS levels and autophagy in HSCs20,78,80, (Fig. 3). Likewise, mitochondrial function, largely regulated by sirtuins, not only affects stem cell functions directly but also causes secondary effects on ROS and nutrient-sensing activities, which further modulate stem cell phenotypes29,30,108,113,184.
Stem cell–autonomous phenotypes, such as DNA and protein damage caused by accumulated toxic metabolites, as well as non-autonomous stresses resulting from extracellular signals, contribute to a decline in stem cell function and depletion of the stem cell pool. However, in some cases at least, these aging phenotypes can be reversed to restore the regenerative function of stem cells. Such restorative interventions hold promise for the treatment of many diseases, including sarcopenia, heart failure and neurodegeneration, although whether these strategies truly restore stem cell function to a youthful state or instead induce a state of ‘pseudo-youth’ in which the reprogrammed cells retain an epigenetic memory of their true age remains an open and important question. Nonetheless, observations of the reversibility of stem cell aging have generated excitement about the development of ‘rejuvenating’ interventions that could extend the healthy years of life. Interventions that hold particular promise include those that target aging mechanisms that commonly affect tissues impaired by age-related diseases and dysfunction. For example, based on studies genetically targeting senescent cells for removal in progeroid mice170, the development of senolytics, compounds that induce (by direct targeting or mobilization of the immune system) the removal of tissue-ensconced senescent cells holds promise for improving stem cell and organ function across a range of tissue systems. Likewise, the demonstration that common blood-borne signals can influence stem cell behavior and aging phenotypes in the muscle, brain and heart, coupled with the accessibility of these circulating mediators for intervention, should encourage further preclinical and translational studies modulating the systemic microenvironment to enhance maintenance and repair in aged tissues. Finally, the availability of nutritional and pharmacological agents that can target derangements in metabolism of aged cells to improve stem cell function and regenerative potential provides another near-term opportunity for new therapeutic strategies. Ultimately, strategies to combat diseases of aging will likely achieve greater success by focusing on high-level integrators of tissue physiology that can evoke remodeling of aging tissue architecture at the cellular and molecular level.
Improving the healthspan of elders takes on increasing urgency as human lifespans continue to increase, and even small gains in healthspan could dramatically lessen the impact of an aging population on the health care system and economy. Although clearly there is much still to be discovered about stem cell function, aging and the pathways to therapy, what we know so far clearly encourages further studies. By continuing to clarify the fundamental mechanisms by which stem cells age, ongoing research will develop interventions that someday may change the way we age.
Edited by corb, 19 February 2016 - 11:02 PM.
