Key result
Disruption or inhibition of 12/15-LOX improved STZ-induced cardiac dysfunction and fibrosis by reducing inflammation and oxidative stress in diabetic mice.
Why the study?
Does inhibition or deletion of 12/15-LOX improve cardiac dysfunction and fibrosis in models of diabetic cardiomyopathy?
Population
Streptozotocin-induced diabetic mice and neonatal cultured cardiomyocytes exposed to high glucose conditions
Comparison
Disruption of 12/15-LOX, administration of… vs Wild-type STZ-induced diabetic mice or untreated…
Design
Preclinical
Authors
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Supports 12/15-LOX inhibition in preclinical diabetic cardiomyopathy; leaves open applicability to patients.
Does inhibition or deletion of 12/15-LOX improve cardiac dysfunction and fibrosis in models of diabetic cardiomyopathy?
Inhibition of 12/15-LOX reduces inflammation and oxidative stress, improving cardiac dysfunction and fibrosis in preclinical models of diabetic cardiomyopathy.
Suzuki et al. (2014) studied Diabetic cardiomyopathy. 12/15-LOX disruption or inhibition vs. Wild-type STZ-induced diabetic mice or untreated controls was evaluated on Cardiac dysfunction, fibrosis, inflammation, and oxidative stress. Disruption or inhibition of 12/15-LOX improved STZ-induced cardiac dysfunction and fibrosis by reducing inflammation and oxidative stress in diabetic mice.
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