Fight Aging!

First generation stem cell therapies, such as those using cells derived from fat tissue, have been shown to reduce chronic inflammation. This effect is produced as a result of signaling from the transplanted cells, which near entirely die rather than surviving to integrate into tissues and perform useful work. Improvements to tissue regeneration and function are much less reliably obtained, however. There are no doubt many other effects of stem cell signaling on native cell behavior, a complicated area of research in which progress is slow an incremental.

Researchers here show that stem cell therapy can upregulate the mitochondrial quality control mechanism of mitophagy. This helps to clear out damaged mitochondria more efficiently, and thereby improve cell function. Mitophagy is known to decline with age for a variety of still poorly explored reasons. Mitochondrial function also declines with age, and multiple lines of evidence suggest that faltering mitophagy is a sizable part of that problem. Stem cell therapies are probably not the most efficient way to address failing mitochondrial function with age, but if they can illuminate specific mechanisms that might be targeted by other means, then this is probably helpful.

Adipose-derived stem cells regulate metabolic homeostasis and delay aging by promoting mitophagy

Tissues undergo a process of degeneration as the body ages. Mesenchymal stem cells (MSCs) have been found to have major potential in delaying the aging process in tissues and organs. However, the mechanism underlying the anti-aging effects of MSC is not clear which limits clinical applications. In this study, we used adipose-derived mesenchymal stem cells (ADSCs) to perform anti-aging treatments on senescent cells and progeroid animal models.

Following intervention with ADSCs, replicative senescence was delayed and metabolic homeostasis was transformed from catabolism to anabolism. Metabolomic tests were used to analyze different metabolites. We found that ADSCs acted to accelerate mitophagy which eliminated intracellular reactive oxygen species and improved the quality of mitochondria. These processes acted to regulate the cellular metabolic homeostasis and ultimately delayed the process of aging. Allogeneic stem cell therapy in a Progeria animal model (DNA polymerase gamma (POLG) knockin, mitochondrial dysfunction) also showed that ADSC therapy can improve alopecia and kyphosis by promoting mitophagy.

Our research confirms for the first time that allogeneic stem cell therapy can improve aging-related symbols and phenotypes through mitochondrial quality control. These results are highly significant for the future applications of stem cells in aging-related diseases.