How Diabetes Affects Blood Vessel Repair Cells
Author Information
Author(s): Seeger Florian Hartmut, Chen Linping, Spyridopoulos Ioakim, Altschmied Joachim, Aicher Alexandra, Haendeler Judith
Primary Institution: University of Frankfurt
Hypothesis
Inhibition of ETS transcription factors can improve the number and function of vasculogenic progenitor cells in diabetes.
Conclusion
Diabetes leads to dysregulated activation of ETS transcription factors, which blocks the functional activity of progenitor cells and their commitment towards the endothelial cell lineage.
Supporting Evidence
- High glucose levels increase apoptosis of endothelial progenitor cells.
- Inhibition of ETS1 expression rescues the reduction of progenitor cell number induced by high glucose.
- Diabetes impairs the functional activity of progenitor cells.
Takeaway
Diabetes makes it harder for the body to repair blood vessels because it affects special cells that help with this process. By changing how certain proteins work, we can help these cells do their job better.
Methodology
The study involved isolating mononuclear cells from blood samples of healthy volunteers and diabetic patients, and using mouse models to analyze the effects of high glucose on progenitor cells.
Potential Biases
Potential bias in patient selection and the use of animal models that may not fully replicate human diabetes.
Limitations
The study primarily focused on specific signaling pathways and may not account for all factors affecting progenitor cell function in diabetes.
Participant Demographics
The study included healthy volunteers and patients with type 2 diabetes, with a mean age of 62 years for the diabetic group.
Statistical Information
P-Value
p<0.05
Statistical Significance
p<0.05
Digital Object Identifier (DOI)
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