Key result
RAGE antagonist FPS-ZM1 reverses methylglyoxal-induced angiogenic impairment in EPCs via the AGE/RAGE-VEGFR-2 pathway.
Why the study?
Dysfunction in bone marrow-derived endothelial progenitor cells contributes to cardiovascular complications in diabetes, but the molecular mechanisms are not fully understood.
Does methylglyoxal induce angiogenic impairment in bone marrow-derived endothelial progenitor cells via the AGE/RAGE pathway?
Does methylglyoxal induce angiogenic impairment in bone marrow-derived endothelial progenitor cells via the AGE/RAGE pathway?
Methylglyoxal induces angiogenic impairment in endothelial progenitor cells via the AGE/RAGE-VEGFR-2 pathway, suggesting a potential therapeutic target for diabetic vascular complications.
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Hypothesis-generating for RAGE antagonism in diabetic vasculopathy; leaves open translation to human outcomes.
Kim et al. (2018) studied Diabetic vascular complications. Methylglyoxal (MG) and FPS-ZM1 was evaluated on Cell viability, VEGFR-2 protein expression, and tube formation. Methylglyoxal induced angiogenic impairment in endothelial progenitor cells via the AGE/RAGE-VEGFR-2 pathway, which was significantly reversed by the RAGE antagonist FPS-ZM1.
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