Key result
sTNFR1 plasmid improves LV function and reduces infarct size in post-MI rats by suppressing TNF-alpha.
Why the study?
Increased circulating and cardiac TNF-alpha levels during myocardial ischemia contribute to impaired LV function and infarct size, but the effect of sTNFR1 gene transfer on cardiac function after myocardial infarction was unclear.
Does sTNFR1 gene transfer improve cardiac function and reduce infarct size in a rat model of myocardial infarction?
Does sTNFR1 gene transfer improve cardiac function and reduce infarct size in a rat model of myocardial infarction?
In vivo transfer of the sTNFR1 gene improves cardiac function and reduces infarct size in a rat model of myocardial infarction by suppressing TNF-alpha bioactivity.
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Does not support clinical use; leaves open whether sTNFR1 gene transfer improves post-MI remodeling in humans.
Sugano et al. (2004) studied Myocardial infarction. sTNFR1 plasmid vs. LacZ plasmid was evaluated on Cardiac function and infarct size. Injection of 200 microg sTNFR1 plasmid in rats post-myocardial infarction suppressed TNF-alpha bioactivity, improved left ventricular function, and reduced infarct size compared to LacZ plasmid.
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