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Review
. 2019 Aug;23(8):4866-4875.
doi: 10.1111/jcmm.14373. Epub 2019 Jun 17.

Save your gut save your age: The role of the microbiome in stem cell ageing

Affiliations
Review

Save your gut save your age: The role of the microbiome in stem cell ageing

Yi Tan et al. J Cell Mol Med. 2019 Aug.

Abstract

The tremendous importance of microbiota in microbial homoeostasis, alterations in metabolism and both innate and adaptive immune systems has been well established. A growing body of evidence support that dysbiosis or compositional changes in gut microbiota is linked to the ageing of stem cells in terms of dysregulations of metabolism, aberrant activation of the immune system as well as promoting epigenetic instability of stem cell. In this concise review, we elucidate recent emerging topics on microbiotic alterations and underlying mechanisms in stem cell ageing.

Keywords: ageing; gut permeability; microbiome; stem cell.

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Conflict of interest statement

The authors declare that they have no competing interests.

Figures

Figure 1
Figure 1
The metabolic programming of quiescent stem cells and differentiated stem cells in terms of the balance between glycolysis and oxidative phosphorylation. The common paradigm is that quiescent stem cells in the niche of normal commensal bacteria tend to prefer glycolysis accompanied with activation of anti‐oxidizing systems. On the contrary, differentiated stem cells under the niche of dysbiosis prefer oxidative phosphorylation rather than glycolysis to promote irreversible proliferation and differentiation of stem cells
Figure 2
Figure 2
Control of intestinal stem cell homoeostasis through crosstalk between immune T cells and the intestinal commensal bacteria. In response to dysbiosis and increased gut permeability caused by ageing, T helper cells are activated to elicit the proliferation and differentiation of intestinal stem cells into Paneth cells and Tuft cells, accompanied with thwarting the functions of regulatory T cells which are responsible for promoting self‐renewal of intestinal stem cells. As a result, the intestinal stem cell pools are exhausted

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