Much of the output of the regenerative medicine and tissue engineering fields will be of greatest use to old people: repair and replacement of worn, damaged, and diseased tissue. Unfortunately the cellular environment in an old body works to suppress stem cell activity, and this seems to be a more important factor in the decline of regenerative capacity than age-related damage to stem cells themselves, or the size of the stem cell population. This is perhaps an evolved response to rising levels of cellular damage, and works to suppress cancer risk - but at the cost of an accelerated decline in organ and tissue function.
From a practical standpoint, this means that the stem cell research community must learn to control and reverse specific aspects of aging in order for their therapies to have the best possible effect. Otherwise they are throwing good stem cells into an environment that will suppress their activity. This roadblock is actually a good thing: this field of research is very well funded, and thus we all benefit as they find out that aging is in their way. Here is an example of the sort of exploratory early-stage work taking place today:
This study investigated whether cytokine enhancement of a biodegradable patch could restore cardiac function after surgical ventricular restoration (SVR) even when seeded with cells from old donors. ... SVR can partially restore heart size and improve function late after an extensive anterior myocardial infarction. However, 2 limitations include the stiff synthetic patch used and the limited healing of the infarct scar in aged patients.
We [placed cytokines onto] porous collagen scaffolds. We seeded human mesenchymal stromal cells from young or old donors into the scaffolds, with or without growth factors. The patches were characterized and used for SVR in a rat model of myocardial infarction. Cardiac function was assessed.
In vitro results showed that cells from old donors grew slower in the scaffolds. However, the presence of cytokines modulated the aging-related p16 gene and enhanced cell proliferation, converting the old cell phenotype to a young phenotype. In vivo studies showed that 28 days after SVR, patches seeded with cells from old donors did not induce functional recovery as well as patches seeded with young cells. However, cytokine-enhanced patches seeded with old cells exhibited preserved patch area, prolonged cell survival, and augmented angiogenesis, and rats implanted with these patches had better cardiac function. The patch became an elastic tissue, and the old cells were rejuvenated.