As we observed with QRS duration, the difference in fibrosis area did not reach statistical significance between Mlc2a Cre /+ ; S1pr1 f /+ hearts and Mlc2a Cre /+ ; S1pr1 f /− mutant hearts.
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Deletion of Sphingosine 1-Phosphate receptor 1 in cardiomyocytes during development leads to abnormal ventricular conduction and fibrosis.
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