Key result
In mice post-myocardial infarction, 11βHSD1 deficiency increased vessel density and improved ejection fraction (P < 0.05) compared with wild-type mice.
Why the study?
Does 11βHSD1 deficiency improve angiogenesis and cardiac function post-MI in mice?
Population
11βHSD1(-/-) and wild-type (C57BL/6) mice with induced myocardial infarction via coronary artery ligation
Comparison
11βHSD1 deficiency (genetic knockout) vs Wild-type (C57BL/6) mice
Design
Preclinical
Follow-up
28 days
Authors
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Supports 11βHSD1 as post-MI target; leaves open human translation and trials.
Does 11βHSD1 deficiency improve angiogenesis and cardiac function post-MI in mice?
p-value: p=<0.05
Genetic deficiency of 11βHSD1 in mice improves angiogenesis, reduces infarct thinning, and preserves cardiac function after myocardial infarction, suggesting a potential therapeutic target.
McSweeney et al. (2010) studied Myocardial infarction. 11βHSD1 deficiency vs. Wild-type (C57BL/6) mice was evaluated on Vessel density and ejection fraction (p=<0.05). In mice post-myocardial infarction, 11βHSD1 deficiency increased vessel density and improved ejection fraction (P < 0.05) compared with wild-type mice.
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