Why the study?
The molecular mechanism by which aminoguanidine reduces advanced glycation end product-associated damage in diabetes is not well understood.
Population
Forty-five male Wistar rats and primary rat myofibroblasts
Comparison
T2DM treated with aminoguanidine vs untreated T2DM and control
Design
Preclinical animal and in vitro study
Follow-up
Up to 25 weeks
Authors
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AG mitigates cardiac fibrosis in T2DM rats; leaves open human translation and requires clinical trials.
Aminoguanidine reduces oxidative stress-associated cardiac fibrosis in a diabetic rat model by modulating AGE/RAGE signaling and downstream fibrogenic pathways.
Magdaleno et al. (2019) studied this question.
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