Key result
Inhibition of ACE activity in genetically obese diabetic mice arrested the increase in blood PAI-1 activity, cardiac PAI-1 and tissue factor mRNA, and coronary perivascular fibrosis.
Why the study?
Does ACE inhibition attenuate hypofibrinolysis and reduce cardiac perivascular fibrosis in genetically obese diabetic mice?
Population
Genetically modified obese mice and lean controls
Comparison
Inhibition of ACE activity initiated at 10 weeks… vs Untreated obese mice and lean controls
Design
Preclinical
Follow-up
20 weeks
Authors
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ACE inhibition may mitigate fibrosis in diabetic obesity models; leaves open human translation and requires prospective trials.
Does ACE inhibition attenuate hypofibrinolysis and reduce cardiac perivascular fibrosis in genetically obese diabetic mice?
ACE inhibition attenuates hypofibrinolysis, augmented tissue factor expression, and coronary perivascular fibrosis in a mouse model of obesity and insulin resistance.
Zaman et al. (2001) studied Obesity and insulin resistance. ACE inhibition vs. Lean controls was evaluated on PAI-1 activity in blood, cardiac PAI-1 and tissue factor mRNA, and coronary perivascular fibrosis. Inhibition of ACE activity in genetically obese diabetic mice arrested the increase in blood PAI-1 activity, cardiac PAI-1 and tissue factor mRNA, and coronary perivascular fibrosis.
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