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- W1600450190 abstract "Introduction: Alterations in calcium homeostasis in the endoplasmic/sarcoplasmic reticulum (ER) can cause stress that ultimately may affect ventricular function. Previously, we reported that α7β1D integrin modified Ca2+ regulatory pathways in the cardiomyocyte via ryanodine receptor 2 (RyR2) stabilization, and offers a means to protect the myocardium from ischemia/reperfusion injury. In the present study, we hypothesized that integrin overexpression (OE) would have beneficial effects against post-myocardial infarction (MI) left ventricular (LV) remodeling via the inhibition of ER stress. Methods: MI was created in 9-12 week old α7β1D integrin overexpressing male mice and age/gender-matched littermate controls by left coronary artery ligation. Groups were followed for 4 weeks post-MI. Results: Survival rate was significantly increased in α7β1D integrin OE mice (90% vs. control, 38.5%, p<0.05). There was no significant difference in LV fractional shortening between both groups (Control 8.7±0.4%, α7β1D 15.8±..." @default.
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- W1600450190 date "2014-11-25" @default.
- W1600450190 modified "2023-09-23" @default.
- W1600450190 title "Abstract 12501: Integrin Overexpression Improves Survival Rate After Myocardial Infarction Through Attenuation of ER Stress" @default.
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