Key result
Administration of the soluble epoxide hydrolase inhibitor TUPS significantly attenuated Angiotensin II-induced cardiac hypertrophy, decreased cardiomyocyte size, and reduced expression of hypertrophy markers in rodent models.
Why the study?
Does soluble epoxide hydrolase inhibition prevent angiotensin II-induced cardiac hypertrophy in rodent models?
Population
Rodent models of angiotensin II-induced cardiac hypertrophy and neonatal cardiomyocytes isolated from rats…
Comparison
Soluble epoxide hydrolase inhibitor, losartan… vs Untreated controls (implied)
Design
Preclinical
Authors
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Caution against clinical use; hypothesis-generating for sEH inhibition in angiotensin II-mediated hypertrophy.
Does soluble epoxide hydrolase inhibition prevent angiotensin II-induced cardiac hypertrophy in rodent models?
p-value: p=<0.05
Inhibition of soluble epoxide hydrolase prevents angiotensin II-induced cardiac hypertrophy in preclinical models, identifying it as a potential therapeutic target.
Ai et al. (2009) studied Angiotensin II-induced cardiac hypertrophy. Soluble epoxide hydrolase inhibitor (TUPS) vs. Vehicle (PEG400) was evaluated on Cardiac hypertrophy (assessed by heart weight to body weight ratio, echocardiography, and hypertrophic marker expression) (p=<0.05). Administration of the soluble epoxide hydrolase inhibitor TUPS significantly attenuated Angiotensin II-induced cardiac hypertrophy, decreased cardiomyocyte size, and reduced expression of hypertrophy markers in rodent models.
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