Why the study?
Does supplemental estrogen prevent cardiac rupture in male C57BL/6J mice with induced myocardial infarction?
Does supplemental estrogen prevent cardiac rupture in male C57BL/6J mice with induced myocardial infarction?
Supplemental estrogen provides cardioprotection against MI-induced cardiac rupture in male mice via MMP-9 reduction and Akt-Bcl-2 anti-apoptotic signaling.
Answers are grounded in this paper and cite their sources.
Hypothesis-generating for estrogen in male mice post-MI; leaves open translation to human cardiac rupture prevention.
In general, young men have a greater risk than age-matched women for many types of cardiovascular diseases, including ischemic heart diseases, such as acute or chronic myocardial infarction (MI)-induced heart failure. The effects of estrogen-replacement therapy in men have not been extensively studied. We evaluated the cardioprotective effects of supplemental estrogen against left anterior descending coronary ligation-induced MI in male C57BL/6J mice. A significantly lower prevalence of cardiac rupture was observed in estrogen-treated mice regardless of castration status. A reduced prevalence of cardiac rupture was associated with decreased activities of matrix metalloproteinase 9 (MMP-9) and increased expression of the anti-apoptotic gene Bcl-2. In vitro studies using H9C2 cells under simulated ischemia re-oxygenation treatment further support the role of estrogen receptor β in estrogen-mediated cardioprotection through the Akt-Bcl-2 signaling pathway.
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Weifeng Shen (2011) studied this question.
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