The Influence of AGEs Environment on Proliferation, Apoptosis, Homeostasis, and Endothelial Cell Differentiation of Human Adipose Stem Cells.

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

• Level A · Stronger Clinical Evidence
• Level B · Emerging clinical evidence with positive signals
• Level C · Early human research exploring benefits
• Level D · Scientific groundwork from lab and animal studies
• Emerging · Emerging topic under active research

Abstract (original English)

The aim of this study was to evaluate the changes of proliferation, apoptosis, homeostasis, and differentiation of human adipose-derived stem cells (hASCs) in the simulated diabetic microenvironment and discuss the potential of the mesenchymal stem cell in the treatment of chronic diabetic wound. We simulated diabetic microenvironment with glycation end products (AGEs) in vitro and studied the changes of hASCs in proliferation and apoptosis. We found that AGEs inhibited the proliferation and lead to hASCs apoptosis, and the endothelial cell directed differentiation was also inhibited. AGEs upregulated growth-related oncogene and monocyte chemoattractant protein-1 and downregulated urokinase-type plasminogen activator receptor, which may inhibit the proliferation and transference of endothelial cells. The simulated diabetic microenvironment affects the proliferation, apoptosis, and homeostasis of hASCs, the endothelial cell migration, and the synthesis of collagen protein, leading to delayed wound healing.

Evidence level

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

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